Veterinary Virology Exam 1 Overview
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List six important ways that viruses impact domestic animals, humans, and science.

  1. Cause significant diseases in animals 2. Cause agriculturally and economically important exotic diseases 3. Cause important zoonotic diseases 4. Induce cancers in animals 5. Responsible for newly recognized diseases 6. Useful as vectors.

Which of the following are general aspects of viral biology that make viruses formidable? (Select all that apply)

  • Highly prone to genomic mutations (correct)
  • Plenty of metabolic machinery
  • Highly stable in the environment (correct)
  • Can evade host defenses (correct)

    • What is one way to mitigate transmission of virus from a primary infected host?

    Isolation of infected host.

    Define 'serotype.'

    <p>A set of viruses that can be distinguished from other viruses in the same species based on antigenic properties.</p> Signup and view all the answers

    What occurs during the 'eclipse stage' of viral replication?

    <p>The virus is uncoating and synthesizing its genome and proteins within a host cell.</p> Signup and view all the answers

    Identify five ways or conditions that inactivate enveloped viruses.

    <ol> <li>Heat 2. Oxidation 3. Freezing/thawing 4. Desiccation 5. Detergents.</li> </ol> Signup and view all the answers

    Which step of viral replication involves binding of the virus to the host cell?

    <p>Attachment</p> Signup and view all the answers

    What is the primary determinant of host cell specificity related to viral infection?

    <p>The appropriate receptor on the host cell that the viral ligand binds to.</p> Signup and view all the answers

    Describe how changing receptor usage can impact viral host range.

    <p>It can result in host range expansion, allowing the virus to infect new species.</p> Signup and view all the answers

    What happens during the biosynthesis step of viral replication?

    <p>Viral proteins are synthesized</p> Signup and view all the answers

    What are virus proteins or gene products?

    <p>Subcomponents of a virus.</p> Signup and view all the answers

    What is a DIVA vaccine?

    <p>A vaccine with gene deletions/markers that help differentiate infected from vaccinated animals.</p> Signup and view all the answers

    Why should live virus and inactivated vaccines generally not be mixed?

    <p>Mixing can reduce the efficacy of viable virus vaccines.</p> Signup and view all the answers

    What is an advantage of replicating vaccines?

    <p>Effective at inducing protective immunity</p> Signup and view all the answers

    What is a disadvantage of non-replicating vaccines?

    <p>Both B and C</p> Signup and view all the answers

    Drugs must be both ______ and effective.

    <p>safe</p> Signup and view all the answers

    What is one barrier to producing effective antiviral drugs?

    <p>Drugs must be both safe and effective.</p> Signup and view all the answers

    What is the mode of action for antiviral drugs that target uncoating?

    <p>They interfere with uncoating.</p> Signup and view all the answers

    What type of antiviral drug is Acyclovir?

    <p>A nucleoside analog.</p> Signup and view all the answers

    What does Tamiflu inhibit?

    <p>Neuraminidase.</p> Signup and view all the answers

    What is the purpose of the 3CL protease in viral replication?

    <p>Responsible for processing viral polyprotein.</p> Signup and view all the answers

    What is the incubation period for systemic viral infections?

    <p>Occurs after secondary (peak) viremia, ~8-9 days post-infection</p> Signup and view all the answers

    Which of the following factors determine whether a virus remains localized or spreads systemically? (Select all that apply)

    <p>Directional release</p> Signup and view all the answers

    Primary viremia is often subclinical or undetectable.

    <p>True</p> Signup and view all the answers

    What contributes to the febrile response during a viral infection?

    <p>Proinflammatory cytokines released by infected cells.</p> Signup and view all the answers

    Secondary viremia usually occurs after approximately ______ days post-infection.

    <p>8-9</p> Signup and view all the answers

    List the three main host defense systems against viral infections.

    <p>Physical and biochemical barriers, innate immune response, adaptive immune response.</p> Signup and view all the answers

    What is the main role of type I interferons in antiviral immunity?

    <p>Protect neighboring uninfected cells from being infected</p> Signup and view all the answers

    Match the following viral infections with their examples:

    <p>Localized infection = Canine papillomavirus Systemic infection = Feline infectious peritonitis (FIP) Severe localized infection = Calf – rotavirus infection</p> Signup and view all the answers

    What is the purpose of attenuated vaccines?

    <p>Reduce virulence but still induce protective immunity.</p> Signup and view all the answers

    Macrophage susceptibility plays an important role in the outcome of viral infection as they can either ingest and kill the virus or become ______.

    <p>infected</p> Signup and view all the answers

    What must replication of all viruses result in?

    <p>Positive (+) sense mRNA</p> Signup and view all the answers

    Why are RNA viruses more prone to developing genomic mutations?

    <p>They do not have a proof-reading mechanism.</p> Signup and view all the answers

    What is viral latency?

    <p>The virus is present but not replicating.</p> Signup and view all the answers

    What does CPE stand for?

    <p>Cytopathic Effects</p> Signup and view all the answers

    What is an example of a mechanism through which DNA viruses promote tumor development?

    <p>Binding to growth factor receptors</p> Signup and view all the answers

    Susceptible cells are those that can produce and release infectious virus.

    <p>False</p> Signup and view all the answers

    List three features of retroviral replication/biology that lend to their ability to cause neoplasia.

    <p>Reverse transcription, integration into host chromosome, and transcriptional regulatory sequences in the viral long terminal repeat (LTR).</p> Signup and view all the answers

    The majority of infections in a population do not result in disease, referred to as the ______.

    <p>iceberg</p> Signup and view all the answers

    Viral encoded proteins important in viral replication are excellent targets for developing antiviral therapeutics.

    <p>True</p> Signup and view all the answers

    What is a major anatomical portal viruses use to enter a host?

    <p>Skin abrasions</p> Signup and view all the answers

    Match the following terms with their definitions:

    <p>Permissive cells = Support complete replication of a virus Abortive infection = Production of progeny virions does not occur Productive infection = Production of new infectious viral particles Cytopathic effect = Virus-induced cellular changes visible by light microscopy</p> Signup and view all the answers

    What are virus proteins or gene products?

    <p>Subcomponents of a virus.</p> Signup and view all the answers

    Define a DIVA vaccine.

    <p>A vaccine with gene deletions/markers that differentiates infected from vaccinated animals.</p> Signup and view all the answers

    Why should live virus and inactivated vaccines generally not be mixed?

    <p>Mixing can reduce the efficacy of viable virus vaccines.</p> Signup and view all the answers

    What are the advantages of replicating vaccines over non-replicating vaccines?

    <p>Effective at inducing protective immunity</p> Signup and view all the answers

    What are some barriers to producing effective antiviral drugs?

    <p>Must be safe and effective.</p> Signup and view all the answers

    Which of the following is a mode of action for direct-acting antiviral drugs?

    <p>Interfere with uncoating</p> Signup and view all the answers

    What is the role of Tamiflu?

    <p>It's a neuraminidase inhibitor that prevents virus release.</p> Signup and view all the answers

    What does Acyclovir target in viral replication?

    <p>Viral polymerases.</p> Signup and view all the answers

    Match the antiviral drug with its action:

    <p>Amantadine/Rimantadine = Interferes with uncoating Acyclovir = Targets viral polymerases Tamiflu = Neuraminidase inhibitor Paxlovid = Protease inhibitor</p> Signup and view all the answers

    List six important ways that viruses impact domestic animals, humans, and science.

    <p>Viruses cause significant diseases in animals, agriculturally and economically important exotic diseases, important zoonotic diseases, induce cancers in animals, cause newly recognized diseases, and are invaluable for studying biological processes.</p> Signup and view all the answers

    Which of the following aspects of viral biology contribute to their formidable nature? (Select all that apply)

    <p>Highly prone to genomic mutations</p> Signup and view all the answers

    What are the five major primary sources of viruses that affect animals?

    <p>Primary infection, zoonotic transmission, environmental infection, persistently infected host, and vector-borne transmission.</p> Signup and view all the answers

    Describe how viruses differ from bacteria in their multiplication.

    <p>Viruses do not replicate by binary fission; they depend on host machinery for replication and lack metabolic machinery to generate energy.</p> Signup and view all the answers

    What is a serotype?

    <p>A serotype is a set of viruses that can be distinguished from other viruses in the same species based on antigenic properties.</p> Signup and view all the answers

    What are the key steps of viral replication? (Select all that apply)

    <p>Biosynthesis</p> Signup and view all the answers

    What occurs during the 'eclipse stage' of viral replication?

    <p>The eclipse stage occurs when the virus is undergoing uncoating, synthesizing its genome and proteins inside the host cell.</p> Signup and view all the answers

    What is the primary determinant of host cell specificity for viruses?

    <p>The appropriate receptor for the virus's viral attachment protein (VAP) is the primary determinant of host cell specificity.</p> Signup and view all the answers

    Which of the following can inactivate enveloped viruses? (Select all that apply)

    <p>Oxidation</p> Signup and view all the answers

    Explain how viral fusion proteins affect tissue tropism.

    <p>Viral fusion proteins influence how effectively a virus can enter a host cell, thereby determining which tissues the virus can infect.</p> Signup and view all the answers

    What is the main difference between localized and systemic viral infections?

    <p>Local infections replicate at the site of entry, while systemic infections spread from that site.</p> Signup and view all the answers

    Secondary viremia is often clinically detectable and occurs after approximately 8-9 days post-infection.

    <p>True</p> Signup and view all the answers

    List the four key factors that govern whether a virus remains localized or spreads systemically.

    <p>Directional release, availability of susceptible cells in deeper tissues, macrophage susceptibility, temperature range of the virus.</p> Signup and view all the answers

    Explain why macrophage susceptibility plays an important role in viral infection outcomes.

    <p>Macrophages can ingest and kill the virus, or if infected, facilitate its spread to many tissues.</p> Signup and view all the answers

    In cases where viruses are released from the apical surface of cells, the infection is likely to be a ______ infection.

    <p>localized</p> Signup and view all the answers

    What effect does hypothermia have on the anatomic site of viral replication?

    <p>It allows the virus to replicate more efficiently in cooler areas, potentially leading to deeper infections.</p> Signup and view all the answers

    Which of the following is considered a first line of defense against viral infections?

    <p>Physical and biochemical barriers</p> Signup and view all the answers

    What roles do type I interferons play in antiviral immunity?

    <p>They are produced in response to viral infection and protect neighboring uninfected cells by inducing an antiviral response.</p> Signup and view all the answers

    Antibodies can neutralize viruses without involving cellular immunity.

    <p>True</p> Signup and view all the answers

    Match the type of antibody-mediated defense mechanism with its description:

    <p>Neutralization = Prevents attachment and penetration of viruses. Opsonization = Facilitates uptake and destruction of viruses. ADCC = Killing cells bound by specific antibodies to viral antigens.</p> Signup and view all the answers

    List one strategy that viruses use to evade the immune response.

    <p>Antigenic variation.</p> Signup and view all the answers

    The main goals of vaccination are to prevent or reduce ______ and reduce transmission.

    <p>disease</p> Signup and view all the answers

    What is the main reason why replication of all viruses must result in the production of positive (+) sense mRNA?

    <p>Positive mRNA is read by the host ribosome for the production of viral proteins.</p> Signup and view all the answers

    Name two strategies that RNA viruses use to produce positive sense mRNA.

    <p>RNA-dependent RNA synthesis and RNA-dependent DNA synthesis (reverse transcription).</p> Signup and view all the answers

    Why are RNA viruses more prone to developing genomic mutations?

    <p>They lack a proofreading mechanism, leading to a higher error/mutation rate during genome replication.</p> Signup and view all the answers

    What is advantageous about having a segmented genome?

    <p>It allows viruses with differing segmented genomes to swap genome segments and create new viruses.</p> Signup and view all the answers

    Which of the following viral proteins are excellent targets for developing antiviral therapeutics?

    <p>RdRp</p> Signup and view all the answers

    What is the definition of cytopathic effects (CPE)?

    <p>CPE refers to virus-induced cellular changes visible by light microscopy.</p> Signup and view all the answers

    How does viral latency influence the choice of diagnostic test?

    <p>A latent virus is non-productive, leading to no observable effects on cells, which requires different diagnostic methods.</p> Signup and view all the answers

    What are the major anatomic portals that viruses use to enter and exit a host?

    <p>Mucosal surfaces, skin abrasions, and vertical transmission.</p> Signup and view all the answers

    List three factors that determine the outcome of viral infection.

    <p>Genetic features of the virus, exposure dose of virus, and host factors.</p> Signup and view all the answers

    What mechanism describes a virus that induces ineffective antibodies?

    <p>Antigenic variation</p> Signup and view all the answers

    Describe how the skin and brain support viral persistence differently.

    <p>The skin has a high threshold of immune activation, while the brain is an immune-privileged site.</p> Signup and view all the answers

    Define transient and persistent viral infections.

    <p>Transient infections are eliminated from the host, while persistent infections are not cleared by the immune system.</p> Signup and view all the answers

    Which of the following mechanisms can viruses use to evade the adaptive immune response?

    <p>All of the above</p> Signup and view all the answers

    List six important ways that viruses impact domestic animals, humans, and science.

    <p>Viruses cause significant diseases in animals, agriculturally important exotic diseases, important zoonotic diseases, induce cancers in animals, responsible for newly recognized diseases, and invaluable for studying biological processes.</p> Signup and view all the answers

    A protective protein shell in which the viral nucleic acid is packaged is called a __________.

    <p>capsid</p> Signup and view all the answers

    Identify how viruses differ from bacteria in their multiplication and energy production.

    <p>Viruses lack metabolic machinery to generate energy and do not replicate by binary fission.</p> Signup and view all the answers

    What are the common nucleic acid types of viral genomes?

    <p>RNA</p> Signup and view all the answers

    All viruses are enveloped.

    <p>False</p> Signup and view all the answers

    Define 'serotype'.

    <p>A set of viruses that can be distinguished from other viruses in the same species based on their antigenic properties.</p> Signup and view all the answers

    What is the function of capsid proteins in viruses?

    <p>Capsid proteins protect the viral genome, assist in binding to host cells, and facilitate uncoating after entry.</p> Signup and view all the answers

    Which of the following factors can inactivate enveloped viruses?

    <p>All of the above</p> Signup and view all the answers

    What is the primary determinant of host cell specificity for viruses?

    <p>The appropriate receptor on the host cell.</p> Signup and view all the answers

    Explain one potential consequence of a virus altering its receptor usage.

    <p>It may expand its host range, allowing it to infect new species.</p> Signup and view all the answers

    What is the main difference between localized and systemic viral infections?

    <p>Localized infections replicate at or near the site of entry, while systemic infections spread from the site of entry.</p> Signup and view all the answers

    What are the incubation period characteristics of localized viral infections?

    <p>Usually have a short incubation period (days to weeks).</p> Signup and view all the answers

    List two key factors that govern whether a virus remains localized or spreads systemically.

    <p>Directional release and availability of susceptible/permissive cells in deeper tissues.</p> Signup and view all the answers

    Why is secondary viremia more diagnostically useful?

    <p>Because there is a higher amount of virus circulating in the blood.</p> Signup and view all the answers

    What are the three main host defense systems against viral infections?

    <p>Physical barriers</p> Signup and view all the answers

    What role do type I interferons play in antiviral immunity?

    <p>Type I interferons induce antiviral responses in neighboring uninfected cells.</p> Signup and view all the answers

    The innate immune response kicks in after days of viral replication.

    <p>False</p> Signup and view all the answers

    What is the primary function of neutralizing antibodies?

    <p>To bind to virions and prevent attachment, penetration, and uncoating.</p> Signup and view all the answers

    What is the main goal of vaccination?

    <p>Prevent or reduce disease</p> Signup and view all the answers

    What are two major contributing factors to the termination of an active viral infection?

    <p>Depletion of susceptible cells and immune response.</p> Signup and view all the answers

    How do cytotoxic T cells help clear viral infections?

    <p>By recognizing viral antigens presented by MHC Class I and inducing apoptosis in infected cells.</p> Signup and view all the answers

    The immune response to viral infections can sometimes contribute to the pathogenesis of __________ diseases.

    <p>viral</p> Signup and view all the answers

    What are virus proteins or gene products?

    <p>Subcomponents of virus, such as protein subunits, VLP, DNA, and RNA.</p> Signup and view all the answers

    Define a DIVA vaccine.

    <p>DIVA vaccines have gene deletions/markers that help differentiate infected from vaccinated animals.</p> Signup and view all the answers

    What is the main reason why live virus and inactivated vaccines should not be mixed?

    <p>Mixing viable virus vaccines with inactivated or subunit/component type vaccines can reduce the efficacy of the viable virus vaccines.</p> Signup and view all the answers

    What are the advantages of replicating vaccines?

    <p>Ability to revert to virulent strain</p> Signup and view all the answers

    What are the disadvantages of non-replicating vaccines?

    <p>No ability for reversion</p> Signup and view all the answers

    What are some barriers to producing effective antiviral drugs for veterinary use?

    <p>Drugs must be safe and effective, need etiologic diagnosis, must be administered early, and are often cost-prohibitive.</p> Signup and view all the answers

    What are the general modes of action for antiviral drugs targeting the virus life cycle?

    <p>All of the above</p> Signup and view all the answers

    What is the function of Tamiflu?

    <p>Tamiflu is a neuraminidase inhibitor preventing virus release.</p> Signup and view all the answers

    What does Paxlovid target?

    <p>Paxlovid targets the viral 3CL protease.</p> Signup and view all the answers

    What stimulates the activation of fusion peptides in envelope glycoproteins?

    <p>Conformational changes triggered by a stimulus.</p> Signup and view all the answers

    What is the difference between low pathogenic avian influenza (LPAI) and highly pathogenic avian influenza (HPAI)?

    <p>LPAI uses localized proteases causing mild disease, while HPAI has ubiquitous proteases resulting in lethal disease.</p> Signup and view all the answers

    Why must all viruses produce positive (+) sense mRNA?

    <p>Positive mRNA is read by the host ribosome for the production of viral proteins.</p> Signup and view all the answers

    Which strategies do RNA viruses employ to produce positive sense mRNA?

    <p>RNA-dependent RNA synthesis</p> Signup and view all the answers

    What is a major reason why RNA viruses are more prone to developing genomic mutations?

    <p>They lack a proof-reading mechanism.</p> Signup and view all the answers

    What are two advantages of a virus having a segmented genome?

    <p>It allows swapping of genome segments and the creation of new viruses.</p> Signup and view all the answers

    What is the term for the process by which a virus introduces its genome into a cell?

    <p>Infection</p> Signup and view all the answers

    Define cytopathic effect (CPE).

    <p>CPE refers to virus-induced cellular changes visible by light microscopy.</p> Signup and view all the answers

    What are the major differences between transient and persistent infections?

    <p>Transient infections are cleared by the immune system while persistent infections are not.</p> Signup and view all the answers

    What are five mechanisms that viruses use to persist in an infected host?

    <p>Evade adaptive immune response</p> Signup and view all the answers

    Define viral latency.

    <p>Viral latency refers to the virus being present but not replicating.</p> Signup and view all the answers

    Match the following mechanisms of viral tumor development with their descriptions.

    <p>Inactivate tumor suppressor gene proteins = Leads to unchecked cell growth Bind growth factor receptors = Stimulates growth signaling pathways Produce oncoproteins = Regulates transcription Integration of dsDNA into host chromosome = Incorporation of viral genetic material</p> Signup and view all the answers

    The majority of infections in a population result in disease.

    <p>False</p> Signup and view all the answers

    What principal factors determine the outcome of viral infection?

    <p>Host genetics</p> Signup and view all the answers

    Study Notes

    Introduction to Viruses

    • Six key impacts of viruses include causing significant animal diseases, economically important exotic diseases, zoonotic diseases, inducing cancers, triggering newly recognized diseases, and serving as vectors in biological studies.
    • Viral transmission is efficient, characterized by high titers, environmental stability, and various transmission routes.
    • RNA viruses exhibit high mutation rates, potentially causing significant disease or enabling cross-species infections.
    • Viruses evade host defenses through mechanisms such as latency and antigenic variation, leading to persistence and potential for new infections.
    • Unlike bacteria, viruses are not affected by common antibiotics and antiviral drugs are limited in availability.

    Sources of Viral Infections

    • Primary infection can spread through reinfection, mitigated by isolating infected hosts.
    • Zoonotic transmission is reduced by minimizing interspecies interactions.
    • Environmental infection severity can be lessened through sanitation and decontamination practices.
    • Persistently infected hosts may require antiviral treatment or supportive care.
    • Vector-borne transmission can be alleviated by implementing preventative measures.

    Virus Structure and Classification

    • Viral genomes can be RNA or DNA, with variations such as linear or circular, single-stranded or double-stranded, and can vary in size from 2kb to over 200kb.
    • Capsids are protective protein shells, while envelopes are lipid membranes derived from host cells containing viral glycoproteins.
    • Enveloped viruses are sensitive to heat, oxidation, freezing/thawing, desiccation, and detergents, making them easier to control through sanitation.
    • Capsid proteins serve as optimal targets for serological testing and vaccine development due to their conservation across virus variants.

    Viral Replication

    • Six key steps of viral replication:

      • Attachment: Virion binds to host cell using viral attachment proteins and host receptors.
      • Penetration: Virus crosses the host cell membrane via direct penetration or membrane fusion.
      • Uncoating: Capsid removal liberates the viral genome by using cellular factors.
      • Biosynthesis: Synthesis of mRNA and replication of viral genome using host cell machinery.
      • Assembly: Viral proteins and genomes coalesce into new virion particles.
      • Release: Non-enveloped viruses lead to cell lysis, while enveloped viruses mature by budding without necessarily killing the host cell.

    • The one-step growth curve represents how time affects infectious virus production, with an eclipse phase when new infectious particles are undetectable.

    Viral Tropism and Host Specificity

    • Viral ligands (attachment proteins) interact with cellular receptors to determine host range and tissue tropism.
    • Changes in receptor usage can lead to broader host ranges and novel diseases; Canine Parvovirus serves as a case study.
    • Key stages in viral replication such as attachment, penetration, and biosynthesis are vulnerable to antibody interference, blocking the infection process.

    Pathogenicity and Virulence Factors

    • Viral fusion proteins and protease activation are critical in influencing tissue tropism and pathogenicity in avian influenza viruses, differentiating high-pathogenic from low-pathogenic strains.

    RNA Virus Replication and Mutations

    • All viruses must produce positive (+) sense mRNA for their proteins to be synthesized by host ribosomes.
    • RNA viruses utilize distinct strategies, like RNA-dependent RNA synthesis or reverse transcription, to generate mRNA.
    • The absence of proofreading mechanisms in RNA viruses leads to higher mutation rates and genetic diversity.
    • Segmented genomes allow for reassortment between different viruses, contributing to viral adaptability and evolution.

    Therapeutic Targets

    • Viral proteins essential for replication present promising targets for antiviral development, as they are specific to viruses and avoid harming host cells.### Antiviral Therapeutics
    • RdRp, RT, and DNA viral polymerases are unique to viruses and serve as prime targets for antiviral drugs.
    • Viral proteases are crucial for processing viral polyproteins during biosynthesis, making them key targets for antiviral treatment.

    Virus-Cell Interactions

    • Susceptible Cells: Have specific receptors for viral attachment, but do not guarantee productive viral infection.
    • Permissive Cells: Support complete viral replication beyond mere attachment; influenced by the host's internal biochemistry.
    • Productive Infection: Occurs when a cell is both susceptible and permissive, leading to the generation of new infectious viral particles.
    • Abortive Infection: Results when a cell is susceptible but not permissive, failing to produce viral progeny.

    Cytopathic Effects (CPE)

    • CPE indicates morphological changes in host cells caused by viral infections, detectable via light microscopy.
    • CPE manifestations include cytoskeletal disruption, syncytia formation, necrosis, apoptosis, and lysis, with cell rounding preceding lysis.
    • Certain CPE are virus-specific, aiding in diagnostics; for instance, syncytial cell formation is associated with several virus families.

    Viral Latency and Tumor Development

    • Viral Latency: Refers to the presence of a virus without replication, leading to no observable cellular effects.
    • DNA viruses can drive tumor development by inactivating tumor suppressor genes, binding growth factor receptors, and producing transcription factors.
    • Retroviruses influence tumor development through mechanisms such as gene acquisition, cellular gene activation, and stimulation of signaling pathways.

    Viral Pathogenesis

    • Pathogenicity: Qualitative measure of a virus's ability to cause disease; determined by both virus and host characteristics.
    • Virulence: Quantitative measure of pathogenicity, focusing solely on the virus's severity.

    Disease Management and Transmission

    • Management practices to maintain a larger “underwater portion of the iceberg” include vaccination, good hygiene, nutrition, and minimizing stress.
    • The virulence of a virus affects clinical outcomes; more virulent infections result in more severe disease manifestations.

    Factors Influencing Viral Infection Outcomes

    • Viral infection outcomes depend on virus genetics, exposure dose, and host characteristics such as age, immune status, nutritional health, and genetic makeup.

    Modes of Viral Transmission

    • Horizontal Transmission: Viruses enter through mucosal surfaces or skin; can lead to iatrogenic (medical procedure-related) transmission.
    • Vertical Transmission: Occurs from dam to offspring, potentially leading to abortion or congenital diseases.

    Transient vs. Persistent Infections

    • Transient Infections: Characterized by complete clearance of the virus within a short duration, following self-limiting mechanisms controlled by the immune system.
    • Persistent Infections: Virus remains in the host and may cause variable disease severity, often with immune evasion strategies in play.

    Mechanisms of Viral Persistence

    • Viruses employ tactics like evasion of the immune response, immune tolerance, tissue-specific infection, and restricted gene expression to persist in the host.

    Immune System Evasion

    • Viruses can induce ineffective antibodies, change neutralizing antigens, and interfere with antigen presentation to evade the adaptive immune response.

    Differences Between Localized and Systemic Infections

    • Localized Infections: Short incubation period, virus replicates near the entry site, and shedding occurs from the same organ.
    • Systemic Infections: Longer incubation, extensive spreading via lymphatic and hematogenous routes, peak viremia coinciding with clinical signs.

    Core Temperature and Viral Replication

    • Changes in body temperature can influence the site of viral replication; cooler areas may promote localized replication, as seen in respiratory or dermal infections.

    Resolution of Viral Infection

    • Termination factors include depletion of susceptible cells (crucial for localized infections) and the immune response (adaptive response predominates in systemic infections).

    Diagnostic Testing for Viral Infections

    • Differences exist in serological response based on mechanisms of persistence; immunologic tolerance often results in no antibodies, whereas latency yields minimal antibody production despite low antigen levels.### Timing Differences: Localized vs Systemic Infections
    • Peak viral replication occurs around days 3-4 for localized infections and days 8-9 for systemic infections.
    • Innate immune response is initiated at day 2 in localized infections, while adaptive immune response begins around day 9-10 in systemic infections.
    • Clinical signs of localized infections appear around day 2, while systemic infections show signs between 8-12 days post-infection.
    • During localized infections, diagnostic samples should be collected around days 2-4, whereas, for systemic infections, they are collected around days 8-9.

    Host Defense Systems Against Viral Infections

    • 1st line of defense: Physical and biochemical barriers at body surfaces (skin, mucociliary clearance, acidity, etc.).
    • 2nd line of defense: Innate immune response, a generalist response activated rapidly upon pathogen recognition.
    • 3rd line of defense: Adaptive immune response, taking days to weeks to develop and resulting in immunological memory.

    Detection of Viral Infections

    • Innate immune system identifies viruses through pattern recognition receptors (PRRs) that detect pathogen-associated molecular patterns (PAMPs).
    • PRR binding triggers a signaling cascade leading to type I interferons (IFNs) and proinflammatory cytokines induction.

    Role of Type I Interferons

    • Type I IFNs (alpha and beta) are rapidly produced within 3-4 hours after viral infection.
    • They protect neighboring uninfected cells by inducing antiviral responses, but do not protect already infected cells.
    • Host-specific nature ensures selective action against viral infections.

    Fever Response During Viral Infection

    • Proinflammatory cytokines released from infected cells lead to febrile responses, which inhibit viral replication and enhance defense mechanisms.
    • Symptoms associated with fever include malaise and flu-like sensations.
    • Caution advised when using anti-pyretics; they should only be used at dangerously high fever levels.

    NK Cells and Phagocytes in Viral Infections

    • NK cells and phagocytes respond quickly (2-3 days) and are not antigen-specific.
    • NK cells destroy virus-infected cells, while phagocytes engulf and degrade viruses.
    • Both cells release cytokines that stimulate adaptive immune response.

    Humoral and Cell-Mediated Immune Responses

    • B lymphocytes produce antibodies, while T lymphocytes (helper and cytotoxic) play distinct roles in enhancing and activating immune response.
    • Humoral immunity targets extracellular viruses, whereas cell-mediated immunity addresses intracellular viruses.

    Antibody-Mediated Host Defense Mechanisms

    • Neutralization: Antibodies prevent virus attachment and entry into cells.
    • Opsonization and Phagocytosis: Antibodies facilitate virus uptake by phagocytes.
    • Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC): Killing of virally infected cells through specific antibodies binding viral antigens.

    Mechanisms of Virus Neutralization by Antibodies

    • Antibodies may block ligand-receptor interactions, inhibit penetration/uncoating, aggregate viral particles, or lead to lysis via complement activation.

    Role of Cytotoxic T Cells

    • Cytotoxic T lymphocytes (CTLs) recognize viral peptides presented by MHC Class I and induce apoptosis of infected cells.
    • Helper T cells assist in the activation of CTLs and enhance the overall immune response.

    Viral Strategies to Evade Immune Response

    • Viruses adopt mechanisms like antigenic variation, preventing apoptosis, evasion through latency, modulating MHC expression, and invoking immune cell destruction.

    Immune Response Pathogenesis

    • In certain infections (e.g., FIP), immune response products can lead to disease symptoms, such as vasculitis from immune complex formation.

    Vaccination Goals and Strategies

    • Vaccination aims to prevent/reduce disease and transmission of viral infections.
    • Vaccines are complemented by quarantine and disinfection for effective control.

    Characteristics of Attenuated Vaccines

    • Attenuated vaccines are derived from avirulent strains that stimulate protective immunity while retaining some viral characteristics and replicative capacity.

    Types of Viral Gene Product Vaccines

    • Types include protein subunit vaccines, virus-like particles (VLP), and DNA/RNA vaccines coding for protective antigens.

    DIVA Vaccines Advantages

    • DIVA vaccines allow differentiation between infected and vaccinated animals through specific markers, improving monitoring and control measures.

    Mixing Vaccines Caution

    • Mixing viable virus vaccines with inactivated or subcomponent vaccines can reduce efficacy due to unintended immune responses.

    Replicating vs Non-Replicating Vaccines

    • Replicating vaccines provide strong immunity but may revert to virulence, while non-replicating vaccines are safer but less effective.

    Barriers to Effective Antiviral Drug Development

    • Antiviral drugs must be safe and effective, with challenges including target specificity, early treatment needs, issues with viral replication in vitro, and high costs.

    Modes of Action for Antiviral Drugs

    • Direct-acting antivirals target stages of virus replication, including uncoating, replication, release, and protein synthesis to inhibit viral lifecycle efficiently.

    Introduction to Viruses

    • Six key impacts of viruses include causing significant animal diseases, economically important exotic diseases, zoonotic diseases, inducing cancers, triggering newly recognized diseases, and serving as vectors in biological studies.
    • Viral transmission is efficient, characterized by high titers, environmental stability, and various transmission routes.
    • RNA viruses exhibit high mutation rates, potentially causing significant disease or enabling cross-species infections.
    • Viruses evade host defenses through mechanisms such as latency and antigenic variation, leading to persistence and potential for new infections.
    • Unlike bacteria, viruses are not affected by common antibiotics and antiviral drugs are limited in availability.

    Sources of Viral Infections

    • Primary infection can spread through reinfection, mitigated by isolating infected hosts.
    • Zoonotic transmission is reduced by minimizing interspecies interactions.
    • Environmental infection severity can be lessened through sanitation and decontamination practices.
    • Persistently infected hosts may require antiviral treatment or supportive care.
    • Vector-borne transmission can be alleviated by implementing preventative measures.

    Virus Structure and Classification

    • Viral genomes can be RNA or DNA, with variations such as linear or circular, single-stranded or double-stranded, and can vary in size from 2kb to over 200kb.
    • Capsids are protective protein shells, while envelopes are lipid membranes derived from host cells containing viral glycoproteins.
    • Enveloped viruses are sensitive to heat, oxidation, freezing/thawing, desiccation, and detergents, making them easier to control through sanitation.
    • Capsid proteins serve as optimal targets for serological testing and vaccine development due to their conservation across virus variants.

    Viral Replication

    • Six key steps of viral replication:

      • Attachment: Virion binds to host cell using viral attachment proteins and host receptors.
      • Penetration: Virus crosses the host cell membrane via direct penetration or membrane fusion.
      • Uncoating: Capsid removal liberates the viral genome by using cellular factors.
      • Biosynthesis: Synthesis of mRNA and replication of viral genome using host cell machinery.
      • Assembly: Viral proteins and genomes coalesce into new virion particles.
      • Release: Non-enveloped viruses lead to cell lysis, while enveloped viruses mature by budding without necessarily killing the host cell.

    • The one-step growth curve represents how time affects infectious virus production, with an eclipse phase when new infectious particles are undetectable.

    Viral Tropism and Host Specificity

    • Viral ligands (attachment proteins) interact with cellular receptors to determine host range and tissue tropism.
    • Changes in receptor usage can lead to broader host ranges and novel diseases; Canine Parvovirus serves as a case study.
    • Key stages in viral replication such as attachment, penetration, and biosynthesis are vulnerable to antibody interference, blocking the infection process.

    Pathogenicity and Virulence Factors

    • Viral fusion proteins and protease activation are critical in influencing tissue tropism and pathogenicity in avian influenza viruses, differentiating high-pathogenic from low-pathogenic strains.

    RNA Virus Replication and Mutations

    • All viruses must produce positive (+) sense mRNA for their proteins to be synthesized by host ribosomes.
    • RNA viruses utilize distinct strategies, like RNA-dependent RNA synthesis or reverse transcription, to generate mRNA.
    • The absence of proofreading mechanisms in RNA viruses leads to higher mutation rates and genetic diversity.
    • Segmented genomes allow for reassortment between different viruses, contributing to viral adaptability and evolution.

    Therapeutic Targets

    • Viral proteins essential for replication present promising targets for antiviral development, as they are specific to viruses and avoid harming host cells.### Antiviral Therapeutics
    • RdRp, RT, and DNA viral polymerases are unique to viruses and serve as prime targets for antiviral drugs.
    • Viral proteases are crucial for processing viral polyproteins during biosynthesis, making them key targets for antiviral treatment.

    Virus-Cell Interactions

    • Susceptible Cells: Have specific receptors for viral attachment, but do not guarantee productive viral infection.
    • Permissive Cells: Support complete viral replication beyond mere attachment; influenced by the host's internal biochemistry.
    • Productive Infection: Occurs when a cell is both susceptible and permissive, leading to the generation of new infectious viral particles.
    • Abortive Infection: Results when a cell is susceptible but not permissive, failing to produce viral progeny.

    Cytopathic Effects (CPE)

    • CPE indicates morphological changes in host cells caused by viral infections, detectable via light microscopy.
    • CPE manifestations include cytoskeletal disruption, syncytia formation, necrosis, apoptosis, and lysis, with cell rounding preceding lysis.
    • Certain CPE are virus-specific, aiding in diagnostics; for instance, syncytial cell formation is associated with several virus families.

    Viral Latency and Tumor Development

    • Viral Latency: Refers to the presence of a virus without replication, leading to no observable cellular effects.
    • DNA viruses can drive tumor development by inactivating tumor suppressor genes, binding growth factor receptors, and producing transcription factors.
    • Retroviruses influence tumor development through mechanisms such as gene acquisition, cellular gene activation, and stimulation of signaling pathways.

    Viral Pathogenesis

    • Pathogenicity: Qualitative measure of a virus's ability to cause disease; determined by both virus and host characteristics.
    • Virulence: Quantitative measure of pathogenicity, focusing solely on the virus's severity.

    Disease Management and Transmission

    • Management practices to maintain a larger “underwater portion of the iceberg” include vaccination, good hygiene, nutrition, and minimizing stress.
    • The virulence of a virus affects clinical outcomes; more virulent infections result in more severe disease manifestations.

    Factors Influencing Viral Infection Outcomes

    • Viral infection outcomes depend on virus genetics, exposure dose, and host characteristics such as age, immune status, nutritional health, and genetic makeup.

    Modes of Viral Transmission

    • Horizontal Transmission: Viruses enter through mucosal surfaces or skin; can lead to iatrogenic (medical procedure-related) transmission.
    • Vertical Transmission: Occurs from dam to offspring, potentially leading to abortion or congenital diseases.

    Transient vs. Persistent Infections

    • Transient Infections: Characterized by complete clearance of the virus within a short duration, following self-limiting mechanisms controlled by the immune system.
    • Persistent Infections: Virus remains in the host and may cause variable disease severity, often with immune evasion strategies in play.

    Mechanisms of Viral Persistence

    • Viruses employ tactics like evasion of the immune response, immune tolerance, tissue-specific infection, and restricted gene expression to persist in the host.

    Immune System Evasion

    • Viruses can induce ineffective antibodies, change neutralizing antigens, and interfere with antigen presentation to evade the adaptive immune response.

    Differences Between Localized and Systemic Infections

    • Localized Infections: Short incubation period, virus replicates near the entry site, and shedding occurs from the same organ.
    • Systemic Infections: Longer incubation, extensive spreading via lymphatic and hematogenous routes, peak viremia coinciding with clinical signs.

    Core Temperature and Viral Replication

    • Changes in body temperature can influence the site of viral replication; cooler areas may promote localized replication, as seen in respiratory or dermal infections.

    Resolution of Viral Infection

    • Termination factors include depletion of susceptible cells (crucial for localized infections) and the immune response (adaptive response predominates in systemic infections).

    Diagnostic Testing for Viral Infections

    • Differences exist in serological response based on mechanisms of persistence; immunologic tolerance often results in no antibodies, whereas latency yields minimal antibody production despite low antigen levels.### Timing Differences: Localized vs Systemic Infections
    • Peak viral replication occurs around days 3-4 for localized infections and days 8-9 for systemic infections.
    • Innate immune response is initiated at day 2 in localized infections, while adaptive immune response begins around day 9-10 in systemic infections.
    • Clinical signs of localized infections appear around day 2, while systemic infections show signs between 8-12 days post-infection.
    • During localized infections, diagnostic samples should be collected around days 2-4, whereas, for systemic infections, they are collected around days 8-9.

    Host Defense Systems Against Viral Infections

    • 1st line of defense: Physical and biochemical barriers at body surfaces (skin, mucociliary clearance, acidity, etc.).
    • 2nd line of defense: Innate immune response, a generalist response activated rapidly upon pathogen recognition.
    • 3rd line of defense: Adaptive immune response, taking days to weeks to develop and resulting in immunological memory.

    Detection of Viral Infections

    • Innate immune system identifies viruses through pattern recognition receptors (PRRs) that detect pathogen-associated molecular patterns (PAMPs).
    • PRR binding triggers a signaling cascade leading to type I interferons (IFNs) and proinflammatory cytokines induction.

    Role of Type I Interferons

    • Type I IFNs (alpha and beta) are rapidly produced within 3-4 hours after viral infection.
    • They protect neighboring uninfected cells by inducing antiviral responses, but do not protect already infected cells.
    • Host-specific nature ensures selective action against viral infections.

    Fever Response During Viral Infection

    • Proinflammatory cytokines released from infected cells lead to febrile responses, which inhibit viral replication and enhance defense mechanisms.
    • Symptoms associated with fever include malaise and flu-like sensations.
    • Caution advised when using anti-pyretics; they should only be used at dangerously high fever levels.

    NK Cells and Phagocytes in Viral Infections

    • NK cells and phagocytes respond quickly (2-3 days) and are not antigen-specific.
    • NK cells destroy virus-infected cells, while phagocytes engulf and degrade viruses.
    • Both cells release cytokines that stimulate adaptive immune response.

    Humoral and Cell-Mediated Immune Responses

    • B lymphocytes produce antibodies, while T lymphocytes (helper and cytotoxic) play distinct roles in enhancing and activating immune response.
    • Humoral immunity targets extracellular viruses, whereas cell-mediated immunity addresses intracellular viruses.

    Antibody-Mediated Host Defense Mechanisms

    • Neutralization: Antibodies prevent virus attachment and entry into cells.
    • Opsonization and Phagocytosis: Antibodies facilitate virus uptake by phagocytes.
    • Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC): Killing of virally infected cells through specific antibodies binding viral antigens.

    Mechanisms of Virus Neutralization by Antibodies

    • Antibodies may block ligand-receptor interactions, inhibit penetration/uncoating, aggregate viral particles, or lead to lysis via complement activation.

    Role of Cytotoxic T Cells

    • Cytotoxic T lymphocytes (CTLs) recognize viral peptides presented by MHC Class I and induce apoptosis of infected cells.
    • Helper T cells assist in the activation of CTLs and enhance the overall immune response.

    Viral Strategies to Evade Immune Response

    • Viruses adopt mechanisms like antigenic variation, preventing apoptosis, evasion through latency, modulating MHC expression, and invoking immune cell destruction.

    Immune Response Pathogenesis

    • In certain infections (e.g., FIP), immune response products can lead to disease symptoms, such as vasculitis from immune complex formation.

    Vaccination Goals and Strategies

    • Vaccination aims to prevent/reduce disease and transmission of viral infections.
    • Vaccines are complemented by quarantine and disinfection for effective control.

    Characteristics of Attenuated Vaccines

    • Attenuated vaccines are derived from avirulent strains that stimulate protective immunity while retaining some viral characteristics and replicative capacity.

    Types of Viral Gene Product Vaccines

    • Types include protein subunit vaccines, virus-like particles (VLP), and DNA/RNA vaccines coding for protective antigens.

    DIVA Vaccines Advantages

    • DIVA vaccines allow differentiation between infected and vaccinated animals through specific markers, improving monitoring and control measures.

    Mixing Vaccines Caution

    • Mixing viable virus vaccines with inactivated or subcomponent vaccines can reduce efficacy due to unintended immune responses.

    Replicating vs Non-Replicating Vaccines

    • Replicating vaccines provide strong immunity but may revert to virulence, while non-replicating vaccines are safer but less effective.

    Barriers to Effective Antiviral Drug Development

    • Antiviral drugs must be safe and effective, with challenges including target specificity, early treatment needs, issues with viral replication in vitro, and high costs.

    Modes of Action for Antiviral Drugs

    • Direct-acting antivirals target stages of virus replication, including uncoating, replication, release, and protein synthesis to inhibit viral lifecycle efficiently.

    Introduction to Viruses

    • Viruses significantly impact animals, humans, and scientific research through disease causation, economic impact, zoonotic potential, cancer induction, emergence of novel diseases, and serving as vectors for biological processes.
    • Virus transmission is highly efficient, capable of reaching high titers, being environmentally stable, and utilizing varied transmission routes.
    • High genomic mutation rates in RNA viruses enable strain development, host species-jumping, and evasion of immune defenses.
    • Viruses persist within hosts, contributing to reinfection risks, with limited tools available for antiviral therapy.
    • Key virus sources impacting animals include primary infections, zoonotic transfers, environmental infections, persistently infected hosts, and vector-borne transmission; mitigation strategies involve isolation, reduced interspecies interactions, sanitation, and antiviral treatments.
    • Viruses exhibit unique structures with capsids (protein shells) and envelopes (lipid membranes); they differ from bacteria in replication, genome composition, and the inability to be treated with antibiotics.
    • Viruses are extremely small, typically measured in nanometers, and require electron microscopy for visualization.

    Virus Structure and Classification

    • Viral genomes vary in type (RNA or DNA), structure (linear or circular), strandedness (single or double), size (2kb to >200kb), and polarity (+, -, or ambisense).
    • Capsids provide protective protein shells for viral nucleic acids, while envelopes include a lipid bilayer and glycoproteins derived from host cells.
    • Enveloped viruses are sensitive to heat, oxidation, freezing/thawing, desiccation, and detergents, which can be exploited for infection control in veterinary medicine.
    • Capsid proteins serve as optimal targets for serological testing and vaccine development due to their conserved nature and immunogenic properties.
    • Serotype defines a virus group identifiable by antigenic properties, with novel serotypes emerging from mutations or recombination affecting viral characteristics and potential consequences.

    Viral Replication

    • Key steps of viral replication: attachment, penetration, uncoating, biosynthesis, assembly, and release, with specific processes occurring at each stage.
    • The eclipse phase denotes a period during viral replication when the virus is not detectable in measurable quantities, as it undergoes uncoating and protein synthesis within the host cell.
    • Viral ligand (VAP) binds to host cell receptors, influencing tissue and host tropism, critical for understanding viral infection dynamics.
    • Changes in receptor usage can lead to expanded host or tissue ranges, illustrated by the emergence of Canine Parvovirus.
    • Antibodies can interfere at multiple stages of viral replication, particularly during attachment and penetration.

    Viral Fusion and Proteolytic Activation

    • Fusion proteins facilitate viral entry by inserting into cellular membranes, influenced by protease cleavage necessary for activation.
    • Low pathogenic avian influenza (LPAI) affects limited tissue due to local protease distribution; high pathogenic avian influenza (HPAI) involves widespread protease distribution leading to severe disease.

    Targeting Viral Replication

    • Positive sense mRNA production is essential as it serves as a template for viral protein synthesis.
    • RNA viruses employ RNA-dependent mechanisms for mRNA synthesis, making them prone to higher mutation rates due to lack of proofreading.
    • Segmented genomes allow for genetic reassortment, providing adaptability and potential for new strains.
    • Viral proteins critical for replication present excellent targets for antiviral development, minimizing effects on host cellular processes.### Antiviral Therapeutics
    • RdRp, RT, and DNA viral polymerases are unique viral enzymes targeted by antiviral drugs.
    • Viral proteases are crucial for processing viral polyproteins during biosynthesis and are also targets for antiviral medications.

    Virus-Cell Interactions

    • Susceptible cells have the correct receptors for viral attachment but do not ensure the production of infectious virus.
    • Permissive cells support complete viral replication beyond attachment due to favorable internal biochemistry.
    • Productive infection leads to the creation of new infectious viral particles.
    • Abortive infection occurs when no progeny virions are produced despite susceptibility, indicating a lack of permissiveness.
    • Cytopathic effect (CPE) involves visible cellular changes due to viral infections, identifiable under light microscopy, including cell lysis, necrosis, and syncytia formation.

    Types of Infections

    • Cytolytic infections cause cell death and characterized CPE can assist in virus diagnosis.
    • Viral latency refers to viruses being present without replication, implying the absence of observable cellular effects.
    • DNA viruses can promote tumor development by producing oncoproteins that inactivate tumor suppressors, activate growth factor receptors, and influence transcription.

    Tumor Development Mechanisms

    • Retroviruses can cause tumors through:
      • Gene acquisition via transduction
      • Activation of cellular genes through insertional or trans-activation
      • Signal transduction activation, prompting cell growth.

    Viral Pathogenesis

    • Pathogenicity indicates a virus's ability to cause disease, while virulence measures disease severity quantitatively.
    • A higher virus virulence shifts disease outcomes, leading to more severe clinical signs.
    • Key factors influencing viral infection outcomes include genetic virus features, exposure dose, age, immune status, concurrent infections, nutritional status, and genetics.

    Viral Transmission Factors

    • DEED principles (Dose, Envelope, Environment, Distance) guide viral transmission risk assessment.
    • Viruses enter hosts primarily via mucosal surfaces, skin, and through vertical transmission from mother to offspring.

    Infections: Transient vs Persistent

    • Transient infections are usually cleared by the immune system with a short duration, while persistent infections are maintained and may lead to variable disease severity.
    • Viral persistence is maintained via mechanisms like immune evasion, tolerance, and restricted gene expression.

    Immune Evasion Tactics

    • Viruses may produce non-neutralizing antibodies, undergo antigenic variation, or disrupt the antigen presentation pathway to evade the immune response.

    Diagnostic Testing Differences

    • For persistent infections via immunologic tolerance, no antibodies are produced, while latently infected individuals may produce few antibodies due to limited viral gene expression.

    Localized vs Systemic Infections

    • Localized infections replicate at or near entry points and exhibit short incubation periods, while systemic infections spread throughout the body, have longer incubation periods, and peak serum viral titers.
    • Primary viremia is typically subclinical; secondary viremia has detectable viral levels and correlates with clinical disease onset.

    Factors Influencing Infection Outcomes

    • The outcome of infections is affected by factors determining whether a virus remains localized or becomes systemic, including the release direction of viral particles and the susceptibility of macrophages.

    Impact of Hypothermia

    • Hypothermia can allow viruses to replicate in cooler areas of the body, potentially shifting infection sites and causing complications, such as pneumonia from Feline herpesvirus in young animals.

    Termination of Viral Infections

    • Active viral infections terminate primarily through the depletion of susceptible cells and the immune response, with resolution factors varying in importance between localized and systemic infections.### Timing Differences in Infections
    • Localized vs Systemic Infections: Localized infections peak viral replication around days 3-4, while systemic infections peak around days 8-9.
    • Immune Responses: Innate immune response activation occurs around day 2 for localized infections; systemic infections trigger adaptive responses by day 9 or 10.
    • Clinical Signs: Signs of localized infections start around day 2, with significant signs by day 4. Systemic infections show symptoms 8-12 days post-infection.
    • Diagnostic Timing: Samples for localized infections are optimal during days 2-4, while samples for systemic infections should be collected around days 8-9.

    Host Defense Systems Against Viral Infections

    • Physical and Biochemical Barriers: These include skin, mucociliary clearance, acid, bile, and natural inhibitors; they repel many pathogens.
    • Innate Immune Response: A generalist response that activates rapidly upon pathogen recognition and induces adaptive immune responses.
    • Adaptive Immune Response: Antigen-specific and may take days to weeks to develop, resulting in immunological memory.

    Detection and Activation of Immune Response

    • Detection Mechanism: Viruses are detected by pattern recognition receptors (PRRs) that recognize pathogen-associated molecular patterns (PAMPs).
    • Type I Interferons: Produced by almost all cells in response to infection, these cytokines act rapidly, inducing antiviral responses in neighboring uninfected cells and helping to slow down the infection.

    Fever and Immune Response

    • Proinflammatory Cytokines: These cytokines lead to fever and increase defensive activities, which contribute to flu-like symptoms.
    • Benefits of Fever: Inhibits viral replication, increases blood flow, and enhances inflammatory responses; anti-pyretics should only be used for dangerously high fevers.

    Role of Immune Cells

    • NK Cells: Quickly respond to viral infections, killing infected cells and secreting cytokines that stimulate adaptive responses.
    • Phagocytes: Involved in degrading viruses and facilitating faster immune responses by clearing viral particles.

    Adaptive Immune Response

    • B and T Lymphocytes: B cells produce antibodies while helper T cells activate B cells and cytotoxic T lymphocytes (CTLs), which kill infected cells.
    • Immune Responses: Humoral immunity targets extracellular viruses, while cell-mediated immunity targets intracellular viruses.

    Antibody-Mediated Host Defense Mechanisms

    • Neutralization: Antibodies bind to viruses, blocking infection and preventing penetration.
    • Opsonization and Phagocytosis: Antibodies facilitate the uptake of viruses by phagocytic cells.
    • Antibody-Dependent Cellular Cytotoxicity (ADCC): Specific antibodies mark infected cells for destruction by immune cells.

    Mechanisms of Virus Neutralization

    • Blocking Interactions: Antibodies prevent viruses from binding and entering cells, and can induce aggregation of virus particles.
    • Inhibition and Lysis: Antibodies can stabilize viral structures and, in combination with complement, lead to lysis of viruses.

    CTLs and Helper T Cells' Roles

    • Cytotoxic T Lymphocytes (CTLs): Recognize viral antigens and induce apoptosis in infected cells through perforins and granzymes.
    • Helper T Cells: Activate CTLs and enhance immune responses through cytokine secretion.

    Viral Evasion Strategies

    • Antigenic Variation: Viruses may change their surface antigens to escape immune recognition.
    • Inhibition of Immune Functions: They can prevent apoptosis, modulate MHC expression, and target cytokines.

    Immune Response and Pathogenesis

    • Feline Infectious Peritonitis (FIP): Caused by the immune response to feline enterovirus mutation leading to tissue damage due to immune complex formation.

    Vaccination Goals and Characteristics

    • Goals of Vaccination: Aim to prevent disease and reduce viral transmission.
    • Attenuated Vaccines: Should induce protective immunity with reduced virulence, achieved through natural strains or experimental mutations.

    Vaccine Types

    • Gene Product Vaccines: Include subunit, VLP, DNA, and RNA vaccines, differing from whole virus vaccines.
    • DIVA Vaccines: Differentiate infected from vaccinated animals using specific gene deletions.

    Antiviral Drug Development Challenges

    • Safety Issues: Creating effective but non-toxic antiviral drugs is challenging due to viral dependency on host cell machinery.
    • Narrow Target Specificity: Limited options for broad-acting antivirals necessitate accurate viral diagnosis.

    Antiviral Drug Mechanisms

    • Direct Action: Antivirals target various stages of viral life cycles, such as uncoating (e.g., amantadine) and replication (e.g., nucleoside analogs like acyclovir).
    • Release Inhibition: Neuraminidase inhibitors, such as Tamiflu, block viral release, while protease inhibitors like Paxlovid target viral protein synthesis.

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    This quiz covers Chapter 1 of Veterinary Virology, focusing on the introduction to viruses. It highlights the significant impacts of viruses on domestic animals, humans, and agriculture. Explore the diseases caused by viruses and their relevance to public health.

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