Medically Important Viruses PDF

medically important viruses important facts abt medically important viruses so small that EM needed for visualization DNA/RNA genome wrapped by viral protein, viral nucleocapsid (can be denatured by heat, bleach NaOCl) with/w/o lipid envelope (herpes simplex 1 has lipid envelope) w...

medically important viruses important facts abt medically important viruses so small that EM needed for visualization DNA/RNA genome wrapped by viral protein, viral nucleocapsid (can be denatured by heat, bleach NaOCl) with/w/o lipid envelope (herpes simplex 1 has lipid envelope) which can be dissolved by detergent or organic solvent disinfectant (alcohol) cannot undergo metabolic activity outside host cells, can only reproduce after entry into host cells and take over metabolic machinery, begin synthesizing own  DNA begin reproduction uses all energy, all AA cell cannot function bc not enough materials to survive -> die can also trigger programmed cell death (apoptosis/necrosis) cannot be grown on artificial culture medium, can only grow in cell culture, chick embryo or animals ideal clinical specimens for virus detection - cells VIRUS IS INSIDE CELLS herpes simplex ~200nm, viruses can be 20nm how viruses replicate (LYTIC CYCLE - cell dies as a result) cell attachment and entry via receptor binding inhaled virus, virus goes to nasopharyngeal mucosa and attaches to cell receptor Sars-Cov2 -> ACE 2 (angiotensin converting enzyme 2) induce endocytosis uncoating and release of nucleic acid in cytoplasm (RNA viruses) or nucleus (DNA virus) transcribe genes and translate structural/non-structural proteins structural proteins - what virus is made of nonstructural proteins - enzymes that help produce viral proteins replication of nucleic acid assembly of nucleic acid and proteins to form new virions release of new virions with/without cell death (usual case) virus w latent cycle, aka cell that doesnt get killed (Herpesvirus genome in closed circular episomes (outsome chromosome) assembled into host chromatin) oncogenic/retro-viruses - viral. genome integrtaed into host genome, in CD4 lymphocyte, most important cell in immune sys (HPapillomaV, HImmunodeficiencyV) how viruses are transmitted contact direct - touch indirect - touch fomite recently contaminated by infected person droplet - 1 meter travel distance (>100um)  aerosol (inhalation) - long distance ( 1st infection smaller viral nucleocapsid seen  secondary infection reactivation of virus in neurons occurs in periods of high stress trigeminal sensory neuron can go into brain and spine, causing encephalitis (inflammation of the active tissues of the brain caused by an infection or an autoimmune response) and death Herpes simplex virus 2 (HSV2) infection  reactivated HSV infection primary infection -> reccurrence throughout entire life reactivated during times of stress HSV infect skin cells -> cell death -> production of ulcer idea for how to culture viruses single monolayer of cells covered in virus culture medium take nasopharyngeal swab/skin vesicle fluid to inoculate after complete replication cycle, cell debris detach hole forms -> virus colony plaque stain cells with gentian violet, plaque shows up  easier to show virus when abundant samples obtained from cell culture then use EM to observe (need to have 10^6 ppm) dying cells -> shrunken, multiple nucleus within one cell (giant cell), detachment quantify neutralizing antibody response titre -> concentration of serum that yields 50% of 100PFU (inhibitory concentration 50) "Foci of CPE" refers to localized areas of cytopathic effects (CPE) observed in cell cultures that have been infected with a virus. Key Differences Feature HSV-1 HSV-2 Primary Site Oral (cold sores) Genital (genital herpes) Transmission Oral-to-oral, oral-genital Sexual contact Symptoms Cold sores, gingivostomatitis Genital sores, painful blisters Reactivation Trigeminal ganglia Sacral ganglia Sites Prevalence More common in the general More common in sexually population active adults VZV (varicella zoster virus) - chickenpox exudation as a result of inflammation (dew on a petal appearance) highly infectious transmitted by aerosol single room, negative pressure later at age of 12 reactivation by stress shingles due to reactivated VZV after primary infection, virus becomes latent in sensory ganglion why reactivated infection? after primary infection, virus travels thru sensory nerves and remain as latent infection in cell bodies within dorsal root ganglion or trigeminal ganglion of cervical, thoracic and lumbosacral nerve roots forming episomes (circular viral DNA genome), activated by triggering factors (fever, physical trauma, stress, hormonal balance, age, immuno suppression) episodic reactivation to lytic infection (skin vesicles, brain, other organs) during periods of stress/immunosuppression TYPES OF HERPES (8 in total) ENTEROVIRUSES very small RNA virus very big family viral interference - a lot of interferons other viral diseases w skin rash as prominent symptom enterovirus - hand foot mouth disease parvovirus B19 - erythema infectiosum infectious mononucleosis like syndrome - fever, sore throat, enlarged lymph nodes, atypical lymphocytes in blood, skin rash (esp after antibiotics) primary cytomegalovirus (CMV)  epstein barr virus (EBV) human herpesvirus 6,7 (HHV 6,7) kaposi sarcoma associated herpesvirus (KSHV, HHV8) primary HIV infection vaccine preventable virus diseases w rash measles (aero trans, highly infectious) varicella (chickenpox, aerosol trans, highly infectious) mumps (rash uncommon) rubella (cause severe foetal disease in pregnancy) mpox (gay men) end of fever n rash VIRAL RESPIRATORY INFECTIOSN SARS COV-2 infection 30kilobases RNA dependent RNA polymerase reproduces entire genome SPIKE is protein on surface PCR targets polymerase and M protein genes and E if theres antibodies against the spike then theres neutralizing antibody 1. SARS-CoV-2 Structure: The spike (S) protein is a critical component of the SARS-CoV-2 virus. It enables the virus to attach to and enter human cells by binding to the ACE2 receptor. 2. Immune Response:  When the body is exposed to SARS-CoV-2, the immune system responds by producing antibodies. These antibodies can target various parts of the virus, including the spike protein. 3. Neutralizing Antibodies: Neutralizing antibodies are a specific type of antibody that can block the virus from infecting cells. They do this by binding to the spike protein and preventing it from interacting with the ACE2 receptor on host cells. 4. Detection of Antibodies: During diagnostic tests for SARS-CoV-2, particularly serological tests (like antibody tests), the presence of antibodies against the spike protein is often measured. If a test shows that there are antibodies specific to the spike protein, it is generally interpreted as evidence that the individual has developed neutralizing antibodies. This is because the immune response that produces antibodies against the spike protein typically includes those capable of neutralizing the virus. N (nucleocapsid protein) protects RNA genome point of care testing - no need to go hopsital lab test, increase fluorescent signal -> positive (find Ct value, high Ct value = low viral load vice versa) many types of coronaviruses that can affect humans intermediate hosts - bushmeat ACUTE BRONCHIOLITIS DUE TO RSV baby will die if not fed childs airways is still not well developed airways r supported by cartilage partial obstruction -> cannot exhale obstruction in acute bronchiolitis due to RSV is primarily caused by edema and mucus production in the small airways (bronchioles) inoculate baby's nasalpharyngeal aspirate into cell line dead cells and multinucleated giant cells (syncytium) seasonality why - neutralizing antibodies drop w time winter -> virus survive better haemophilus influenzae is bacteria that does not cause influenza common coinfecting bacteria NA - neuraminidase INFLUENZA VIRUS genome separated into 8 sections 2 proteins on surface haemagglutinin - attaching virus to human host cells for entry neuraminidase - enzyme that detaches linkage usually we only have 2 types of influence H1N1, H3N2 before 1967 seasonal influenza was H2N2, genome reassortment w avian H3Nx, forming human pandemic H3N2 bc we lack antibodies to counter H3N2 recently, point mutation in haemaglutinin (mutations every 3 years -> seasonal outbreak) influenza genome changes by reassortment with animal strains and point mutation many subtypes after vaccine, neutralizing antibody decreases in 4 months  4 -> encephalitis, myocarditis middle airway -> tracheitis, bronchitis lower -> bronchiolitis adenovirus, influenza - ALL regions r ok (common causes of viral pneumonia) MERS -> camel VIRAL GASTROINTESTINAL INFECTION stool pH very low 4-5 rotavirus - cause enterocytes to be unable to abs glucose so bacteria in intestine ferments glucose into lactic acid stool becomes acidic, causing skin corrosion in diapers  milk proteins cannot be abs so coagulated by acid -> milk curds seen in diaper non-enveloped, spokes of the wheels appearance OTHER DIARRHEAL VIRUSES all bc of lacking hand hygiene FEVER Dengue fever secondary infection more deadly (haemorrhagic fever) low mortality rate (primary infection)  Filovirus (like silk) can cause haemorrhagic fever common in Africa Marburg and Ebola virus ARBOVIRUS rhabdovirus - dog bite arbo - arthropod borne cancers associated w virus