• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/31

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

31 Cards in this Set

  • Front
  • Back
Retroviridae Properties
Enveloped, spherical
(+) ssRNA "diploid"
reverse transcriptase
A,B,C,D type particles
Simple and Complex viruses
Simple Retroviral Genomes
GAG: group antigen gene (capsid)
POL: polymerase (reverse transcriptase)
ENV: envelope glycoprotein gene
LTR: long terminal repeat (promotor)
Complex (HIV) retroviral genome
additional proteins on top of simple retroviruses
used for activation, regulation, and infection of virus
HIV life cycle: attachment/penetration
HIV attaches to CD4 cell
VAP is gp120-gp41
viral RNA carried to nucleus
HIV life cycle: Replication
reverse transcriptase makes DNA copy of viral genome, integrating it into host cell genome
LTR is promotor, produces mRNA which is exported from nucleus
HIV life cycle: Assembly and release
RNA forms w/ viral proteins to form RNP capsid
it associates w/ matrix protein and buds through plasma membrane
Simple Retrovirus Gene Expression
3 main structural genes (gag, pol, env)
LTR initiates transcription into mRNA
protease cleaves mRNA into mature proteins
Complex Retrovirus Gene Expression
LTR begins transcription, splicing of regulatory proteins occurs
proteins are made and then aid in virus processing and exit
AIDS Infection
HIV stage 3: confirmed HIV, CD4+ <200 / CD4+ % of total lymphocytes <14
Lenitiviruses
slow viruses in Retroviridae
cause immune difficiency, hematopoietic and CNS disorders
HIV-1 and HIV-2
Origin of HIV
virus strain ZR59 isolated in Kinshasa, Congo 1959
came from Buntu male monkey
HIV pathogenesis
tropism for CD4 expressing T-cells
uses CCR5 and CXCR4 co-receptors
can be passed through sexual intercourse, anal and vaginal
Course of Infection: Acute
virus production
lymphadenopathy and flu-like symptoms
virus and Ag detectable in blood
CMI reduces viremia
Course of Infection: Asymptomatic
3-4 weeks post infection, can last years
latency, viremia decreases
increased viral load=closer to AIDS
Course of Infection: Development of AIDS
when CD4+ cell drop below 500 cell/ul
headache, weight loss, increased infections
increase in viremia and decrease in CD8+
Course of Infection: Late Stage
increase in virulence properties, expands to new cells
rapid replication, enhanced neurotropism
Host response to HIV
10% have AIDS in 2-3 years
80% have AIDS in 10 years
10-17% have AIDS in no less than 20 years
replication occurs best in activated T-cells
Immune System Response: CD4+ cell dysfunction
causes decreased IL-2 production, reduced overall IR
can also cause inappropriate IR
Immune System Response: CD8+ cell dysfunction
abnormally high following infection, to make up for less CD4+
later, a decrease in CD8+ because no cytokines are released to trigger them
Immune System Response: monocyte/macrophage cell dysfunction
defects in chemotaxis, inability to proliferate T-cells, Fc-receptor fxn
Immune System Response: NK cell dysfunction
depend on IL-2, if no cytokine then no NK cell IR
leaves body susceptible to other infections
Humoral IR
Ab against HIV are made early, can neutralize virus early
ineffective against later viral isolates
Cellular IR
CD8+ cytotoxic lymphocytes against HIV slow disease progression, but a rapid drop in CD8+ activity occurs during end stage
AIDS associated Illnesses
Kaposi's Sarcoma: cancer from HHV-8
B-cell Lymphoma: 100X more common in HIV patients than normal, HHV-8 and EBV common factor
HIV Lab Diagnosis
EIA or ELISA
Western Blot
PCR
HIV Treatment: Attachment Inhibitors
Neutralizing Ab: against gp40/gp120
Pfizer: binds to CCR5
HIV Treatment: Fusion Inhibitors
Fuzeon: binds to glycoprotein 120 in HIV surface
HIV Treatment: Nucleoside Reverse Transcriptase Inhibitors
Lamivudine, Tenofovir, Zidovudine
reverse transcriptase incorporates these analogs into DNA, causing disruption of replication
HIV Treatment: Integrase Inhibitor
Efavirenze
prevents integration of viral cDNA into host cell genome
HIV Treatment: Protease Inhibitors
drugs block proteolytic processing of viral sub-units, disrupting production
HIV Treatment: Circumcision
possible 50% reduction in acquiring HIV