14 - HIV - notes.docx

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University of Toronto St. George
Molecular Genetics and Microbiology
Alan Cochrane

FEB 10, HIV-1 replication and TB, malaria, HIV – biggest molecular causes of death Mid-age adults dying – leaving orphans to raise themselves or by other relatives – social change HIV cases – many are women – worldwide HAART =/= cure – there are side effects – life long - No cure, no vaccine - Treatment Cause: zoonosis – transmission of infection from one species to another; like measles from cattle - Was in simian population – transmitted to human beings - Chimpanzees have SIVcpz – related to HIV - Old world monkeys all have SIV – new world monkeys do not o African monkeys developed this virus after dispersal of monkeys around the world - Blood to blood exchange from chimpanzee blood to cut on human o Chimpanzees hunted for food - People did die – but local infections – no spread beyond the village - But with the colonization and roads, railways, expansion of people – urbancentres – spread of the infection from local areas into urban centres and from there o Ex. Prostitution  Virus follows route of migration  Truck drivers and migrant workers carry the virus after being infected with sex with prostitutes  Then spread world wide Modes of transmission - Transfusion based – essentially eliminated - IV drug use – major - Tattooing - All sex is a risk - Part of T cell – first si months of newborn’s immune system is naive, protected by mother’s immune system o Mother’s infected T cells may transfer to newborn Females 7x more susceptible Level in blood of person at time of transmission – higher viral load, higher transmission - Can occur in acute phase – infected person does not yet know - Having a sexual infection increases chances of transferring HIV o Because inflammation caused by the sexual infection, recruit more T cells – susceptible to HIV Viral entry - Insertion of virus into mucosal space – allows virus to interact with mucosa of vagina, anus, penis - Virus bypasses epithelial barrier to get at cells – facilitated by micro tears that allow virus to bypass barrier - Dendritic cells designed to identify and present to immune system novel antigen to warn – they are major traffickers of HIV Different tissues have different susceptibility - Vagina – has thick – changes in size depending on menstrual cycle o Drugs that may change menstral cycle can narrow that barrier – easier to transmit the virus  Ex. Norchamp? o Major entry is cervix – single layer of cells - Men o Penis – hard surface b/c large level of sequmous epithelium o Anus – single layer of epithelial cells Viral transmission - Not efficient - Huge barrier to virus getting through o In semen versus in bloodstream o Actually one or two virions that establish the infection  But enough to kill you Cells virus is targeting is four cell types - T cells - Macrophages and dendritic cells - Infect both T cells and macrophages productively; not so in dendritic cells - DC-sign on dentridic cells – aggravate virus on surface of DC – can enter via endosomes o DC will present all virus to T cells under condition maximal for infection of T cell Once through epithelial barrier, DC present HIV to local T cells in the area – more T cells, higher probability get contact, replicate virus in T cell, traffick into local draining lymph node, which is rich in T cells and amplify the infection – release from local LN and released into circulation When in circulation – hone to all hte T cell rich areas in body – see all immune organs – LN, spleen, thymus - attack first GUT associated lymphoid tissues, which is richest source of T cell Lymphoid tissue – Peyer’s patches rich in T cells and B cells – basically designed to control bacteria sitting in gut – that is their main function - This zone is what HIV will attack Red is T cell – within weeks of infection, virus kills 90% of T cells in Peyer’s patches - Some rebound in blood - Organ slowly or not at all recuperates o Gut immune system severely crippled, won ‘t be restored In blood - CD4 positive T cells dip – once immune system reacts, reduces virus down – some recovery of the T cells in the system, the blood 0 to 12 weeks – nothing or cold-like symptoms Virus comes down to viral load set point – lowest point – clinically latent Higher load set point, faster will progress, Reducing level of CD4 in blood – wearing away on immune system Opportunistic infections that are cause of death b/c immunoincompetent High low set point 2% lucky – die of natural ca
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