05c: Retroviruses/HIV Flashcards
HTLV-1 and HTLV-2 are examples of (X) viruses that cause which diseases?
X = retroviruses;
T-cell leukemias (HTLV = human T-cell leukemia virus)
HIV-1 and HIV-2 are examples of (X) viruses that cause which diseases? Which strain is less virulent?
X = retroviruses;
AIDS (HIV = human immunodeficiency virus); HIV-2 less virulent
T/F: The DNA sequence that defines HIV-1 is most related to that which defines HIV-2.
False - no such thing as “single” DNA sequence that defines HIV
Retroviruses are (enveloped/non-enveloped) viruses, about (X) nm in diameter.
Enveloped;
X = 100
Retrovirus structure: inner shell is composed of (X) proteins and inner core composed of (Y) proteins. What’s contained within the core?
X = matrix Y = capsid
- Genome (2 copes of (+) sense mRNA)
- Proteins (Reverse transcriptase, Integrase, Protease)
T/F: HIV-1 genome is more complex than most retroviruses.
True - Encodes additional gene products (regulate virus replication and play role in pathogenesis)
HIV: The (X) gene product functions as transcriptional transactivator. It can be released from infected cells and induce which processes in uninfected cells?
X = tat
- Alter gene expression
- Apoptosis
HIV: The (X) gene product downregulates CD4 and MHC-1 expression.
X = nef
Long-term non-progressors of HIV (are/aren’t) viremic. Some harbor HIV-1 variants that have mutant of (X) gene product.
Are (but not pathogenic);
X = nef
Worldwide, most common method of HIV-1 transmission is:
M to F sex contact
What are the routes of HIV-1 infection?
- Sexual
- Parenteral
- Perinatal
Primary receptor for HIV-1 is (X), found on (Y) cells. Which viral protein attaches to (X)?
X = CD4 Y = T-helper lymph and macrophages
gp120
The major HIV-1 co-receptors are (X).
X = CCR5 and CXCR4
HIV-1 establishes low-level infection in which cell types?
- DCs
2. Langerhan’s cells
T/F: Macrophages are the cells thought to facilitate HIV-1 dissemination from mucosa to lymph nodes.
False - DCs and Langerhan’s cells
Individuals thought to be resistant to HIV-1 infection are (homo/hetero)-zygous for which gene alteration?
Homozygous;
Deletion in CCR5 gene
A group of long-term non-progressors of HIV-1 expresses high levels of (X), which compete with the virus for (Y).
X = chemokines (MIP-1a, MIP-2b, RANTES) Y = CCR5 binding
List the steps in HIV-1 life cycle that have been targeted by anti-retroviral drugs.
- Receptor binding
- Entry
- Integration
- Proteolytic maturation
HIV-1: (X) co-receptor is expressed on T-cells and macrophages. (Y) co-receptor is preferentially expressed on T-cells.
X = CCR5 Y = CXCR4
HIV-1: drugs block entry of virus into cell by preventing (X) from..
X = gp41
Adopting fusion-competent conformation
Reverse transcriptase synthesizes (X) from (Y). AZT and other anti-retroviral drugs block this step via which mechanism?
X = dsDNA Y = ssRNA
They’re nucleoside analogs that compete with normal nucleoside (terminate DNA chain elongation)
Non-nucleoside inhibitors of reverse transcriptase function as anti-retroviral drugs via which mechanism?
Bind RT near active site and block its activity
HIV-1: lack of proofreading activity of (X) polymerase(s) contribute to viral variants.
X = RNA-dependent DNA Pol (reverse transcriptase) and RNA polymerase II
T/F: HIV-1, like most retroviruses, cannot productively infect non-dividing cells.
False
For most retroviruses, entry of DNA into nucleus requires (X). HIV-1 has (Y) protein that allows DNA transport in absence of (X).
X = nuclear membrane breakdown (during cell division) Y = CA
T/F: Assembled HIV-1 virions, released from cell, are mature.
False - contain uncleaved polyproteins (must undergo proteolytic maturation)
High rates of (X) during HIV-1 infection result in extensive sequence heterogeneity and outgrowth of viral strains with higher (Y) capacity.
X = replication, mutation, and recombination Y = replicative and pathogenic
In acute HIV-1 infection, there’s a sudden drop, followed by rebound increase, in (CD4 cells/viral load).
CD4 cells
In acute HIV-1 infection, there’s a sudden spike, followed by sudden drop, in (CD4 cells/viral load).
Viral load
In acute HIV-1 infection, (CD4 cells/viral load) initially spikes. (X) cells also spike, but then steadily decline.
Viral load;
X = HIV-1 specific CTL
During latent phase of HIV-1 infection, replication is (stopped/slow).
Still very high! (10^8 to 10^9 virions/day)
List examples of HIV-1 induced T-cell abnormalities.
- Lack of Ag response
- Impaired proliferation
- Impaired IL-2 expression (T cell growth)
- Shift from Th1 (CM) to Th2 (humoral) profile
List examples of HIV-1 induced macrophage abnormalities.
Impaired chemotaxis, phagocytosis, and cytokine production
List the general mechanisms by which HIV-1 kills.
- Direct killing (cytotoxicity)
- Syncytium formation
- Immune attack/apoptosis
Worldwide HIV-1 epidemic has epicenters in which countries?
- Sub-saharan Africa
- India
- China
- Russia
T/F: Significant exposure to body fluids from HIV+ person has 30% transmission risk.
False - 0.3%! (Very low).
30% transmission risk for HBV
CDC recommends primary assay for HIV test that detects (X).
X = HIV p24 Ag and HIV Ab
CDC recommends secondary assay for HIV test. If primary assay is (negative/positive), the secondary assay detects (X). What’s the point of this second assay?
X = HIV-1/HIV-2 Ab
Differentiate between HIV-1 v. HIV-2
T/F: Patients can opt-out of screening tests for HIV.
True
T/F: Written consent is required for HIV testing.
False - general consent for medical care is sufficient
List some side effects of HAART.
- Fat redistribution
- Hypercholesterolemia
- Other specific drug adverse effects
