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HIV

QuestionAnswer
General characteristics of HIV Retroviridae Lentivirus genus HIV-1 99% cases in europe & USA HIV-2 mainly west Africa HIV-1 and HIV-2 40% homology HIV-1 3 phylogenetic clades, M N O. MAIN NON-MAIN and OUTLIER. Majority of subtypes in main group
Epidemiology Infection with HIV-1 - AIDS 1.8 million deaths, 27-60 million people affected worldwide
Pathogenesis AIDS- complex of signs and symptoms associated with HIV, characterised by the presence of rare and opportunistic pathogens in the presence of anti-HIV antibodies.
Transmission Unprotected sex Mother to child transmission (verticle, in utero, during delivery, in breastmilk) IV drug use
Infection pattern Initial contact - virus infects dendritic cells at muscosal surface before infecting CD4+ T cells. These T cells become activated facilitating release and spread of virus. Reservoirs established in lymphoid tissue (GALT LN)
Infection pattern cont. Years later Cd8+ cells respond - already chronic HIV production. Adaptive immune response reduces HIV levels dramatically, CD4+ cells destroyed over 5-10 years, HIV levels rise and opportunistic pathogens infect
Particle and genome structure 2 copies of +ve sense ssRNA genome enclosed by cone shaped capsid surrounded by host derived lipid envelope 9.7kb genome 9 genes encoding 16 proteins
LTR Contains control region which bind transcription factors initiating transcription
gag polyprotein processed into matrix, capsid, nucleocapsid and a budding protein
pol encodes viral enzymes which process other HIV genes, includes RT
env produces gp160 protein which is cleaved into gp120 and gp41. gp120 - CD4 and co-receptor binding, gp41 - mediates fusion
VPR facilitates infection of macrophages
VPU promotes CD4 degredation allowing viral release from cell (similar to neuraminidase)
Vif overcomes unknown cellular inhibitory effects
Nef promotes CD4 and MHC1 downregulation, blocks apoptosis, enhances viral infectivitiy, alters state of cellular activation
Rev regulates viral gene expression through deactivation viral splicing machinery allowing incomplete spliced transcripts
tat enhances RNA pol II, binds to LTR
Receptors CCR5 - Macrophages CXCR4 - T helper cells
Mechanisms of HIV killing Formation of giant cells with multiple nuclei through interaction with gp120, gp41 and CD4 + co-receptors Accumulation of unintegrated forms of linear viral DNA Proapoptotic effects of Tat, nef and VPR Metabolic burden of HIV replication
Mechanisms of HIV killing 2. Expression of nef alone as a transgene in mice confers loss of immunity and death of CD4+ cells
Disease progression Can be acute (2-5 years) slow (long term non progression (5-10 years) elite controllers (20 year+)
Disease progresssion 2. Viral factors: virus copy number and set point (stable viral load within an individual) virus fitness (rapid changing of genome, fitness can be advantageous or disadvantageous e.g increased expression of Nef) Host - 32bp deletion in CCR5- HIV reduction
Patient treatment and antivirals CD4+ <200 patients started on HAART (highly activate antiretrovial therapy) targets - RT, HIV proviral DNA, integrase, protease, TAT antagonists. targets identifed by producing double negative mutants - found TAT REV and GAG are essential Nucleos
Created by: teemo616
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