Viral Pathogenesis: Principles and Mechanisms

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Questions and Answers

What is viral pathogenesis?

The methods to prevent viral infections

The classification of viruses based on their pathogenicity

The processes by which viral infections cause diseases (correct)

The study of viral replication

What is tropism in the context of viral pathogenesis?

The process of viral replication within the host cell

The mechanism by which viruses evade the immune system

Susceptibility, permissiveness, and accessibility of cells to viral infection (correct)

The ability of viruses to mutate rapidly

Where do DNA viruses typically replicate?

In the cytoplasm of the host cell

In the endoplasmic reticulum

In the nucleus of the host cell (correct)

Within the cell membrane

What are some common points in the virus life cycle shared between all pathogenic viruses?

Release of new virions, antigenic variation, and morphological changes Signup and view all the answers

What is the outcome of failed virus infection?

Viral genome unable to complete replication Signup and view all the answers

What is the outcome of lytic non-cytocidal infection?

Complete virus replication occurs, but cell remains alive Signup and view all the answers

Which virus is latent in sacral or lumbar ganglia?

Herpes simplex virus (HSV) Signup and view all the answers

What is the global prevalence of HSV-1 in 0–49-year-olds?

66.6% Signup and view all the answers

Which virus is the causative agent of genital herpes?

Herpes simplex virus (HSV) Signup and view all the answers

Where does HSV-1 establish latency?

Trigeminal ganglia Signup and view all the answers

What occurs during reactivation of HSV?

Virion formation and release of new viruses Signup and view all the answers

What type of genes are immediate early (IE) genes in HSV pathogenesis?

Responsive to a viral protein called VP16 Signup and view all the answers

Where does HSV-2 establish latency?

Sacral or lumbar ganglia Signup and view all the answers

What are the clinical symptoms associated with primary HSV-2 infection?

Gingivostomatitis, pharyngitis, tonsilitis, and genital herpes. Signup and view all the answers

What happens during latency of HSV?

Retention of viral genome without production of infectious virions. Signup and view all the answers

What is the function of LAT genes during latency in herpes simplex virus (HSV) infection?

Inhibit apoptosis and promote survival of infected cells Signup and view all the answers

Which viral protein inhibits type I interferon-mediated responses in infected cells during HSV infection?

Virus Host Shut Off Protein (vhs) Signup and view all the answers

What is the primary mode of transmission for human papillomavirus (HPV)?

Direct sexual contact Signup and view all the answers

Which HPV types are associated with cervical cancer?

HPV-16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, and 68 Signup and view all the answers

What is the genome type of human papillomavirus (HPV)?

Circular double-stranded DNA (dsDNA) Signup and view all the answers

"Glycoprotein E" of HSV has which ability?

Fc binding ability. Signup and view all the answers

During latency in herpes simplex virus (HSV) infection, what happens to the viral lytic genes?

They are repressed. Signup and view all the answers

What can cause reactivation of herpes simplex virus (HSV) from latency?

UV light, stress, fever, tissue damage Signup and view all the answers

How does Human Papillomavirus (HPV) transmit through direct contact?

Infects epithelial cells of the skin and mucous membranes Signup and view all the answers

What is the association between HPV-16 and HPV-18 with cervical squamous neoplasia?

Their E6 and E7 gene products inactivate normal functions of p53 and Rb proteins. Signup and view all the answers

What can HPV infection cause?

Benign overgrowth of cells into warts and dysplasia that can become cancerous. Signup and view all the answers

Study Notes

The genes associated with latency (LAT) are expressed when a virus enters latency.
During latency, only the LAT genes are expressed, and all other viral lytic genes are repressed.
Expression of LATs inhibits apoptosis (programmed cell death), promoting the survival of infected cells.
Latent viral episomes bind to the cellular chromatin.
Herpes Simplex Virus (HSV) employs multiple strategies to evade the immune system:
- Virus Host Shut Off Protein (vhs) and Infected Cell Protein 0 (ICP0): inhibit type I interferon-mediated responses in infected cells.
- Glycoprotein C: binds and inactivates C3b component of complement.
- Glycoprotein E: has Fc binding ability.
- HSV encoded protein ICP47 binds to the MHC class I TAP transporter, inhibiting transport of virus peptide and presentation to the immune system.
HSV can reactivate from latency due to cellular factors and external stimuli, such as UV light, stress, fever, tissue damage, and immune suppression.
Reactivation can occur in the absence of clinical symptoms, and HSV-2 sheds virus during asymptomatic reactivation, which is a significant means of transmission.
Human Papillomavirus (HPV) is a non-enveloped virus with a circular, ds DNA genome between 6.8kb and 8.4kb.
HPV is ubiquitous, and up to 80% of people are exposed to it.
HPV is classified into over 200 types, and causes benign to potentially malignant proliferative lesions.
HPV is the fourth most common cancer among women globally, and high-risk HPV types (HPV-16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, and 68) are associated with cervical cancer.
HPV transmits through direct contact, particularly sexual contact.
HPV infection causes cell proliferation, and some HPV types can progress to malignancy through genome integration and continued cell replication, along with accumulating mutations.
HPV-16 and HPV-18 are associated with cervical squamous neoplasia due to their E6 and E7 gene products, which inactivate normal functions of the p53 and Rb proteins, respectively.
HPV oncogenic transformation is coincident with the integration of papillomavirus DNA into cellular DNA and the expression of E6, E7 without virus production, which may lead to neoplasia and eventually metastasis.
HPV infects epithelial cells of the skin and mucus membranes and replicates according to the stage of epithelial cell differentiation.
HPV can cause benign overgrowth of cells into warts, and some HPV types are associated with dysplasia that can become cancerous.

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Description

Explore the principles of viral pathogenesis and mechanisms of viral infections causing diseases, including latency, transformation, chronic infection, and evolution of viruses to evade the immune system.