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41 Cards in this Set

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T8 Cells
AKA CD8 cells, cytotoxic T-lymphocytes (CTL), Tkiller cells. Upon binding to its antigen (on surface of infected cell) AND receiving helper signals from T4 cell, THEN:
1) proliferates
2) kill infected cells
3) moves on to next target
T4 Cells
AKA CD4 Cells, T-helper cells.
In addition to TCR, also have CD4.
Upon binding to its antigen on the surface of an antigen presenting cell, THEN:
1) proliferation
2) secretes cytokines (helper signals) to stimulate B-cells and T8 cells
HIV Specific Characteristics
RNA Virus
a) lentivirus
Retrovirus structure
1) RNA genome 10 kb long. SS RNA. Diploid, 2 copies. 9 genes. Coated with nucleocapsid protein (p7).
2) enzymes, RT, integrase, protease
3) capsid - protein coat, p24
4) lipid envelope. Supported by matrix protein p17. gp = gycloprotein (protein decorated with sugars)
Virus Life Cycle
Production of new viral components
Assembly of components
Genome (9 genes)
1) gag- structural proteins (p24, p17, p7)
2) pol enzymes- RT, integrase, protease
3) env- envelope proteins gp 120, gp41
4) tat - upregulates transcription
5) rev- controls alternative splicing of HIV mRNA. Shift production from early products to late products
How HIV kills T4 cells
1) CTLs (T8 cells) kill infected T4 cells
2) cell-cell fusion leads to synctium. gp120 binds, gp41 facilitates fusion
3) budding excessively
4) insertion of the provirus in a critical gene and cause a lethal mutation
5) apoptosis of T4 cells
Window Period
Timbe between moment of infection to time person has detectable level of antibodies in blood. 6 weeks to 1 year
Appearance of antibodies in blood. 50% seroconvert in 3 months, 90% in 6 months
Stages of Disease Progression
Acute stage
Asymptamatic stage
Chronic symptomatic stage
Acute Stage
30% ppl have no symptoms.
Symptoms occur 2-8 weeks after infection and last 1-4 weeks
Acute retroviral syndrome (ARS). fever, fatigue, weight loss, headaches, sore throat, muscle aches, rash, vomitting, diarrhea, swollen lymph nodes (lymphadenopathy).
CNS infection through mavrophages carrying across blood-brain barrier
Asymptomatic Stage
Usually the longest, 10-12 years without drugs.
Viral load declines due to humaral and cellular response. "Latent" stage but 10-100 billion viruses being produced a day. T4 cells dying at rate of 1 billion/day.
Seroconversion occurs
Chronic Symptomatic stage
AIDS Related Complex (ARC)
lasts few months to years.
defined by number of T4 cells, 200-400.
Increasing viral load leads to symptoms.
Wastiing syndrome. Extreme weakness, fever, night sweats.
Lymphodenopathy returns.
Neurological disease, dementia, spinal cord damage, damage to peripheral nerves in arms and legs.
Opportunistic infections
AIDS stage
T4 cell count less than 200 cells/ml
All previous symptoms still present
Without HAART, individual has 2-3 years
Early stages
1) candida
2)hairy leukoplakia
Yeast. If fungi single celled, then be definition a yeast. Candidiasis starts in mouth then goes to esophagus, called thrush. Vaginal in women. Treated by flucomazola. Symptoms, redness, swelling, cracking, burning, itching, white furry patches of yeast
Hairy Leukoplakia
Looks like thrush. white flurry patches on tongue. caused by epstein barr virus. only seen in AIDS patients. overgrowth of papillae cells of tongue. occurs on sides of tongue, cant be scraped off
Rash on torso, painful. Caused by vericella zoster. Treated with acyclorir
Late infections
Systemic mycoses
AIDS Related Dementia
1/2 AIDS patients get it.
Directly caused by AIDS.
HIV in macrophages and extracellular space. Does not infect neurons, but does kill them. Direct killing, toxic viral proteins secreted by infected cells (gp120, tat).
Indirect killing - bystander cell damage (inflammation). ROS (reactive oxygen species, free radicals).

Symptoms- apathy, depression, insomia, loss of muscle control, seizures, coma, death.
patient losing 2 billion T4 cells/day and body can't keep up with replacing them
Why HIV can't be cured
Memory T4 cells. If it has a latent infection, drugs can't target it. Viral reservoir. The infection can reactivated years or decades later.
Problems with drugs
Drug resistance because HIV mutates so rapidly.
Side effects, some are life threatening.
Compliance, how carefully the patient takes the drug according to the prescription
Constant monitoring of viral load and T4 count
Viral reservoirs in body
Types of Drugs
RT inhibitors - nucleoside analogs and non-nucleoside RT inhibitors.
Protease inhibitors
Fusion inhibitors
Integrase inhibitors
RT Inhibitors
Nucleoside analogs (NRTI) nukes.
Analog is molecule that mimics another.
A nucleoside is sugar and base. Precursor to nucleotide which is made by adding 3 phosphates
Analog incorporated into growing DNA during reverse transcription. It is defective for elongation and leads to chain termination
RT has an affinity for AZT. More likely to pick up AZT than thymamine.
Side effects - vomiting, diarrhea, headaches, rash, chills, fever, inhibiton of mtDNA pol leads to lactic acidosis which leads to decrease of ph in blood, myopathy (wasting), neuropathy (tingling and pain in nerves that eventually go numb), inhibition of stem cell proliferation in bone marrow leads to anemia, inflammation of pancreas, fatal allergic reaction
RT Inhibitors Resistance
RT must stop using AZT. Mutation in the gene necessary so amino acid change in protein. Must change pol gene to change protein.
Bind directly to RT. Nevirapine- used to prevent vertical transmission. More effective, cheaper, shorter regimen, dose to mom during labor and dose to child 3 days later and no vertical transmission.
Side effects- rash, dizzy, insomnia, sleepy, vivid dreams, mood alteration, cant think clearly, liver damage, fatal allergic reaction.
Protease Inhibitors
When virus buds from cell it has to change shape of capsid to be infectious. Done be protease cutting both enzymes aprt and cutting capsid proteins. If process is prevented, then no progeny made and not infectiors. Prevents transmission from cell to cell. have to take many pills a day.
Side effects- intestinal disruption, liver damage, diabetes, heart disease, lypodystrophy syndrome
Lypodystrophy syndrome
Fat redistributed. Lose fat from face, butt, arms, legs and goes to belly and back
Protease Inhibitors Resistance
Has to be 1 or more mutations in pol that changes protease enzyme to lead to drug resistance
Fusion Inhibitors
Target gp41. Drug is 36 amino acid peptide. HRI - heptad reapt 1, forms an alpha helix. 2 helices wound around each other = HR2 heptad repeat 2
Drug is a peptide which mimics HR2, the C region
Trimer of hairpins = six bundle helix
Few side effects
Fusion Inhibitors Resistance
Change in gp41. Need mutation in env gene
Alternative Drug Strategies
Integrase inhibitors. Attachment inhibitors - block binding of gp120 with CD4 or block binding of gp41 with CXCR4 or CCR5.
Highly active anti-retroviral therapy. Drug cocktails, at least 3 drugs.
Common combo = 2 NRTIs, 1 NNRTI, 1PI
Reduce viral load 90% in 2 months. Undetectable in 6 months. Start of HAART is T4 count less than 350 and viral load more than 30,000
Post Exposure Prophylaxis (PEP)
Used for healthcare workers exposed to HIV. Treat with HAART within 72 hours. Take for 4 weeks. Prevents infection
Problems with HIV vaccine
Need both humoral and cellular immunity.
Limitation of animal models
Mutation rate
Viral variability (clades)
Vaccine Types (by function)
1) Preventative vaccines- memory cells, T and B cells
2) Therapeutic vaccine, given after infection. Prevents progression of disease
Whole Killed (inactivated) Virus
Take virus, treat with chemicals or heat to inactivate virus, virus cannot replicate. Not considered a viable option for HIV due to fears of not deactivating all virus
Live attenuated virus
viable, not pathogenic leads to genuine infection to activate cellular immune response. Has been successful in primate studies but also causes disease. Delete nef gene
Viral Subunit Vaccine
pieces of virus that are non-infectious. Safest approach. Proteins injected (ex. envelope spike gp120 usually, gp41). Will not cause cellular immunity. ONly get ceullular immunity with intracellular infection.
DNA Vaccine
Takes genes of HIV in DNA form, put in plasmid and inject into patient. DNA gets into nuclei into host cells. Genes transcribed and translaed leads to host cell making ciral proteins which leads to cellular response
Live vector vaccine
Vector is a carrier of DNA or gene. Render a carrier virus harmless through genetic engineering. Adenovirus and canary pox/ Insert 1 or 2 HIVE genes into carrier virus which leads to HIV proteins in host cell which leads to cellular immunity. "Trojan horse"
Combination vaccine
Subunit and live vector
DNA vaccine and live vector. Known as prime boost