Virology Basics - Structure, Function, & Host Response Flashcards Preview

DD & BL Unit III / Final Exam > Virology Basics - Structure, Function, & Host Response > Flashcards

Flashcards in Virology Basics - Structure, Function, & Host Response Deck (37)
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Eclipse Period of a one-step growth curve

The period of time between 0 and 12 hours after virus adsorption; represents the time period when virus particles have broken down after penetrating cells, releasing their genomes; no infectious virus is detectable inside or outside of the cell


Latent period of a one-step growth curve

The time it takes from the initiation of infection to the release of new infectious virus particles from the cell


(+) ssRNA viruses (5 examples)

"Ribosome ready" - can be directly translated on the (+) mRNA strand by host ribosomes

RdRp are packaged within the virion to replicate the viral genome

Hepatitis A
West Nile
Hepatitis C


(-) ssRNA viruses (5 examples)

RdRp contained within the virion must copy (-) RNA into (+) RNA prior to becoming "ribosome ready" for translation; RdRp can also replicate the viral genome



dsRNA viruses (1 example)

RdRp contained within the virion acts on the (-) RNA to make "ribosome ready" (+) mRNA




(+) stranded RNA virus with a DNA intermediate

(+) ssRNA is copied into dsDNA via reverse transcriptase; viral dsRNA then integrates into the host cell DNA where it is transcribed into mRNA by host RNA polymerase II

Reverse transcriptase comes fully assembled within the viral particle


Tissue tropism

The propensity of a virus to infect certain tissues and not other, determined by viral access to the tissue, receptors required for virus binding and try, expression of host genes required for virus replication, etc.

Ex: enterotropic viruses replicate in the gut, neurotropic viruses replicate in the nervous system



The capacity of a virus to cause disease, determined by genes that affect the virus' ability to replicate, modify host defense mechanisms, cause direct toxicity to cells, etc.


Acute local viral disease

Usually caused by infections of epithelial cells of mucosal surfaces; virus replication & shedding occurs primarily within the original site of infection

Usually involves viruses that mutate rapidly and have many different serotypes; therefore, re-infection is common

Characterized by short incubation periods (1-2 days) and strong IgA immune response


Acute systemic viral disease

Primary infection occurs in epithelium but virus breaches local barriers (basement membrane, connective tissue, etc.) to cross into hematological / lymphatic system; viremia results in secondary replication at various sites, often lymphoid organs, lung, liver

Incubation period is usually 10-21 days; shedding may take place from the epithelium as well as multiple systemic sites

Infection results in lifelong immunity mediated by secretory IgA and serum IgG


Persistent viral infection

Viral infections that continue to produce new viral particles over a long period of time

Ex: Hepatitis B


Latent (reactivating) infection

Viral infections in which periods of little gene transcription and disease may be interrupted by re-initiation of transcription and replication to produce new virus particles


Mechanisms of virus-induced immunopathology (6)

Antigen-antibody complex disease mediated by complement

Cell-mediated responses and destruction - innocent bystander effect

Virus-induced inflammation - acute phase response

Virus induced immune suppression

Antibody dependent enhancement of infection

Virus-induced autoimmunity


Viral transmission - enveloped vs. non-enveloped

Enveloped viruses are fragile and sensitive to environmental stresses; they are most often transmitted by close contact

Non-enveloped viruses can sustain drying, low pH, detergents, and high temperatures; they are often transmitted via respiratory and oral/fecal routes, or fomites


Transforming viral infections

Viruses that contribute to tumorigenesis via activation of oncogenes, inactivation of tumor suppressors, or DNA breakage; may be mediated by either retroviruses or non-retroviruses

Some persistent viral infections may cause ongoing inflammation and so contribute to tumorigenesis


3 outcomes of viral infection

1. Abortive infection - failed infection, no virus produced, no effects on cell

2. Lytic infection - results in production of virus and death of the infected cell

3. Persistent infection - chronic, latent, or transforming


Cytopathic effect

Any detectable morphologic changes in the host cell, caused by viral infection; examples include:

Cytoplasmic vacuolization
Chromosomal breakage
Inclusion bodies
Negri bodies



Cell fusion


Negri bodies

Protein & RNA in the cytoplasm


Permissive vs. Non-permissive

Permissive cells provide the machinery and components required for completion of viral replication; non-permissive cells do not


Mechanisms of viral-mediated cell damage
Direct vs. Indirect

Direct - diversion of cell's energy, shut off of macromolecular synthesis, competition of viral mRNA for cellular ribosomes, etc.

Indirect - integration of the viral genome, induction of mutations in the host genome, inflammation, host immune response, etc.


Type I IFNs


Antiviral cytokines transiently produced and secreted by most infected cells within hours of infection


Type II IFNs


Produced by T cells and NK cells


Role of interferons in production of an anti-viral state

Cells respond to IFNs produced by neighboring infected cells through receptors that signal through Jak/Stat pathways; this affects regulation of transcription factors which control gene expression through interaction with interferon-dependent DNA regulatory elements


Intracellular restriction factors (2 examples)

Cellular proteins that can block post-entry steps of certain viral infections

Trim5 blocks retroviruses

APOBEC blocks HIV and HCV - APOBEC incorporates itself into virus particles, damaging the genetic material of the virus; it can be inhibited by HIV protein Vif, which binds APOBEC and targets it for destruction


Anti-viral stage

Characterized by altered transcription of IFN-responsive genes resulting in a temporary blockade of cell proliferation (p21), reduced cellular metabolism, increased expression of antigen presenting molecules (MHC-I), induction of apoptosis (procaspases), etc

This is a readiness state - the responding cell need not be infected and the products of IFN-induced genes often depend on viral dsRNA as a co-factor in order to ensure that they are only active under conditions of infection


Mediators of the anti-viral state (2)

Protein Kinase R (PKR) - synthesized as an inactive precursor induced by the anti-viral state; activated by dsRNA to phosphorylate and thereby inactivate a cellular translation initiation factor; results in decreased protein synthesis

2'-5' oligoadenylate synthetase (OAS) - synthesized as an inactive precursor induced by the anti-viral state; activated by dsRNA to stimulate a cellular ribonuclease that degrades RNA


Important anti-viral TLRs

TLR3 - recognizes dsRNA
TLR7 - recognizes viral RNA
TLR 9 - recognizes unmethylated CpG


Mechanisms of virus evasion of host defenses (7)

Antigenic variation - antigenic drift / shift

Immune tolerance - virus proteins that closely resemble host proteins

Restricted expression of viral genes - "going invisible" to host defenses (latent infection)

Production of viral molecules that act as inhibitors of host defense molecules

Down regulation of host proteins, i.e. MHC-I

Infection of immunoprivileged sites, i.e. Brain

Direct infection of the immune system

Inhibition of apoptosis and cell cycle control


Antigenic Drift

Gradual change within the same subtype of a virus that occurs through a slow series of mutations in amino acids constituting the hemagluttinin or neuraminidase surface antigens

Occurs after a viral strain has become established in humans as an adaptation to the development of host antibodies