Term
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Definition
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Term
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Definition
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Term
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Definition
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Term
| Does usual viral taxonomy represent viral phylogeny? |
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Definition
| No (ie, viruses are usually classified according to size, structure, genome type, etc., and not according to function or evolution) |
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Term
| What percentage of the human genome was derived from viral elements? |
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Definition
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Term
| What are the stages of the early viral growth cycle? |
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Definition
1. Attachment
2. Penetration
3. Uncoating
4. Replication |
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Term
| During what phase of the viral growth cycle are viral genes expressed? |
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Definition
| Both early and late phases |
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Term
| How is attachment mediated in HSV-1, HIV-1, and influenza A? |
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Definition
| Virus |
Viral protein |
Host receptor |
Host coreceptor |
| HSV-1 |
Envelope proteins |
Heparan sulfate |
Immunoglobulins |
| HIV-1 |
gp120, gp41 |
CD4 |
CCR5 (chemokine receptor) |
| Influenza A |
Hemagglutinin |
Sialic acid |
- |
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Term
| Of HSV-1, HIV-1, and influenza A, which viruses affect most cells of the body? |
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Definition
| HSV-1 and influenza A (HIV-1 is mainly limited to CD4+ T cells) |
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Term
| How does influenza A enter the host cytoplasm? |
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Definition
| Endocytosis; low pH in endosome triggers the synthesis of a fusion protein, which causes fusion. Involves a conformational change in hemagglutinin. |
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Term
| What are the two general ways that HIV-1 can enter the cytoplasm? |
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Definition
| Either like influenza A (via endosome) or by direct fusion with the plasma membrane |
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Term
| Mechanism by which HIV-1 envelope fuses with host plasma membrane |
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Definition
1. gp120-CD4 interaction
2. gp120's fusion peptides are exposed
3. Interaction with CCR5 coreceptor
4. 6-helix bundle formed |
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Term
| Mechanism of action of Fuzeon (aka T-20) |
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Definition
| Inhibits the fusion of the HIV-1 envelope with the host plasma membrane |
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Term
| Purpose of M2 protein on influenza A |
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Definition
| Allows for acidification of virus after it has been endocytosed; acidification allows for uncoating |
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Term
| Mechanism of action of amantadine |
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Definition
| Inhibits M2 protein of influenza A, preventing viral acidification and preventing uncoating |
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Term
| HIV-1 protein that stays behind at the plasma membrane following uncoating |
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Definition
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Term
| HSV-1 component that remains on plasma membrane following viral uncoating |
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Definition
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Term
| HSV-1 tegument protein that enters host nucleus and activates RNA pol II |
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Definition
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Term
| Are viral genes expressed before or after viral replication? |
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Definition
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Term
| Where does transcription and replication occur within a cell infected with influenza A? |
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Definition
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Term
| What protein transcribes (-)ssRNA to mRNA in influenza A? |
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Definition
| Viral polymerase (which hijacks 5' caps from host mRNAs as primers) |
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Term
| Of the viruses HSV-1, HIV-1, and influenza A, which can be treated with inhibitors of DNA synthesis? |
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Definition
| HSV-1 and HIV-1, because influenza A infections don't involve DNA synthesis |
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Term
| How can DNA synthesis be pharmaceutically inhibited in HIV-1 and HSV-1 infections? |
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Definition
| AZT for HIV-1 and acyclovir in HSV-1 |
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Term
| The effects of AZT and acyclovir are limited to what cell types in HIV-1 and HSV-1 infections, respectively? |
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Definition
* AZT is toxic to all cells, regardless of whether they are infected
* Acyclovir is specific for HSV-1-infected cells because it requires activation by a viral thymidine kinase |
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Term
| Initial treatments for HIV-1 mainly targeted what? |
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Definition
| Reverse transcriptase (agents included zidovudine [AZT] and didanosine [ddI]) |
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Term
| HIV-1, HSV-1, and influenza A proteins that target the host plasma membrane |
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Definition
HIV-1
* gp120
* gp41
HSV-1
* Glycoproteins
Influenza A
* HA
* NA
* M2 |
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Term
| How do HIV-1's gag and pol attach to the host plasma membrane during assembly of the virion? |
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Definition
| Via fatty acids (lipid anchors) |
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Term
| How does influenza A's M1 protein attach to the plasma membrane during viral assembly? |
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Definition
| Via M1's hydrophobic sequences |
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Term
| Characteristics of the maturation process in HIV-1 development |
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Definition
| Maturation is the cleavage of precursor polyproteins (eg, gag-pol) into viral enzyes; occurs just before or during release of virions |
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Term
| General class of drugs that prevents HIV-1 maturation |
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Definition
| HIV-1 protease inhibitors (eg, Ro 31-8959) |
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Term
| Typical components of highly active antiretroviral therapy (HAART) |
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Definition
| Two reverse transcriptase inhibitors and one protease inhibitor |
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Term
| How does HSV-1 DNA incorporate into viral capsid? |
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Definition
| Specific DNA-nucleocapsid binding inside host nucleus |
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Term
| How does influenza's A genome associate with the capsid? |
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Definition
| M1 protein translocates to host nucleus where it binds specifically to viral RNA |
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Term
| How does the HIV-1 genome incorporate into the viral capsid? |
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Definition
| The 5' Ψ (psi) integration signal, a secondary structure on HIV-1's genomic RNA, binds specifically to gag |
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Term
| How does the host cell remain alive when HSV-1, HIV-1, and influenza A virus particles exit en masse? |
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Definition
| Viral particles bud outward by a process similar to exocytosis, allowing the host cell to seal small nicks in the membrane following each particle's exit |
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Term
| From which cellular structures do HSV-1, HIV-1, and influenza A gain their envelope? |
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Definition
* HSV-1: nucleus
* HIV-1: plasma membrane
* Influenza A: plasma membrane |
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Term
| How do HIV-1 and influenza A viruses attempt to prevent reinfecting the cell from which they have budded? |
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Definition
* HIV-1 downregulates CD4 expression
* Influenza A's neuraminidase cleaves sialic acid |
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Term
| Two neuraminidase inhibitors |
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Definition
* Zanamivir
* Oseltamivir (Tamiflu) |
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Term
| How is release usually regulated for many viruses? |
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Definition
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Term
| How can HIV-1 infect cells that don't express CD4? |
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Definition
* Use alternative receptor
* Transcytosis (analogous to how influenza A infects cells) across epithelium can deliver HIV-1 to bloodstream
* Injury to barrier |
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Term
| Following entry into CD4- cells, what cell types are most commonly infected by HIV-1? |
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Definition
* Macrophages
* Lymphocytes
(Because they're close by) |
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Term
| Dendritic cells are thought to play a role in the early dissemination of what virus? |
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Definition
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Term
| Is DC SIGN, a receptor found on Langerhans cells, a receptor for HIV-1? |
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Definition
| No, it's a trans-receptor capable only of carrying HIV-1. It doesn't allow HIV-1 to infect the Langerhans cell. |
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Term
| What dendritic cell protein allows dendritic cells to disseminate HIV-1 particles to T cells? |
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Definition
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Term
| Which is more capable of infecting epithelial cells, HIV-1 or HSV-1? |
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Definition
| HSV-1, by far (HIV-1 is generally not able to infect epithelium) |
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Term
| After infecting epithelial cells, does HSV-1 infect nearby or distant cells? |
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Definition
| Typically nearby sensory neurons; distant infections occur so rarely as to be clinically insignificant |
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Term
| What RNAs are required for HSV-1 to establish a latent infection? |
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Definition
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Term
| In what cell types does HSV-1 replicate prior to establishing a latent infection? |
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Definition
* Satellite cells
* Neurons |
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Term
| How does HSV-1 travel between neurons? |
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Definition
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Term
| Transmission of HSV-1 to the CNS is a risk factor for what disorder? |
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Definition
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Term
| Typical location of influenza A infections |
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Definition
| Epithelia of upper respiratory tract |
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Term
| From which side of the cell (apical or basolateral) are HSV-1, HIV-1, and influenza A released? |
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Definition
* HSV-1: basolateral
* HIV-1: basolateral
* Influenza A: apical |
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Term
| Proteolytic cleavage of which influenza A protein allows for ready transmission to neighboring epithelial cells? |
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Definition
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Term
| Is viremia a prominent feature during the ongoing replication phase of an HIV-1 infection? |
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Definition
| No; during this time, T cells are able to keep the viral load down so that viremia is not prominent. |
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Term
| Four mechanisms of immunodeficiency in HIV-1 infection |
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Definition
* Direct (eg, massive budding)
* Apoptosis (viral protein-triggered)
* Innocent bystander (infection of neighboring cells)
* Anergy (viral-protein-triggered) |
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Term
| In what organ system are CD4+ T cells most affected? |
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Definition
| Gastrointestinal system (because it hosts more than 50% of body's T cell population) |
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Term
| How can HIV-1 promote neoplasia? |
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Definition
| One way is for HIV-1's genome to be integrated adjacent to a cellular oncogene |
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Term
| Define viral incubation period |
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Definition
| Time before signs and symptoms of disease become obvious |
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Term
| Do influenza and retroviruses cause acute or persistent infections? |
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Definition
* Influenza: acute
* Retroviruses: persistent |
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Term
| Trivia about the Spanish flu |
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Definition
* 1918-1919
* Killed 20-40 million globally
* Also called La Grippe
* H1N1
* Primarily killed healthy young adults |
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Term
| Are hemagglutinin and neuraminidase encoded on the same or different segments of RNA in the influenza A genome? |
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Definition
| Each is coded by its own segment |
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Term
| Reassortment of different hemagglutinin and neuraminidase isotypes is an example of antigenic shift or antigenic drift? |
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Definition
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Term
| Point mutations in hemagglutinin or neuraminidase of influenza A are examples of antigenic shift or antigenic drift? |
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Definition
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Term
| How often does influenza A exhibit antigenic drift and shift? |
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Definition
* Antigenic drift: every several years
* Antigenic shift: 10-20 years |
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Term
| Persistent viral infections are usually mediated by viruses with what types of genomes? |
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Definition
| Genomes that exist as DNA during the viral replication cycle (eg, herpes and HIV-1, but not influenza A) |
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Term
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Definition
| Diseases that can be transmitted between humans and other vertebrates |
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