Human Immunodefficiency Virus Flashcards
HIV
a Lentivirus, retroviridae
2 subtypes: hiv-1 & hiv-2
target host cell: CD-4 + cells
Sexual, parenteral, vertical
Cross species infections by simian viruses in rural africa
HIV virulence factor
gp120 - attachment protein
gp41 - fusion protein
Reverse transcriptase - converts RNA to DNA
Integrase - incorporates viral DNA - host DNA
Protease - cleave the viral Gag & Gag-pol
polypeptide precursors to form the
mature Virion
HIV findings
Phase 1- acute HIV infection
Phase 2- clinical latency
Phase 3- acquired immunidefficiency
syndrome (AIDS)
Phase 1
Acute HIV infection
2-4 wks after exposure
Viremia
Flu-like symptoms, lymphadenopathy
-/>500 CD4 + cell/uL
Immune response depletes viral numbers in the plasma
Phase 2
Clinical latency
Asymptomatic HIV infection or chronic HIV
infection
Virus reproduces at very low levels
CD4+ declines & virus increases
200-499 CD4+ cells/um
Phase 3 AIDS
<200 CD4+ cells /um or presence of at least 1 AIDS defining condition
1- protozoa: toxoplasma gondii
2- fungi: candida albicans
3- bacteria: mycobacterium avium
intracellulare
4- viruses: cytomegalovirus
Plasma viral load
Best predictor of long term clinical outcome
CD4+ cell counts
Best predictor of short term risk of an oppurtunistic disease
HIV diagnosis
EIA or ELISA TEST (screening)
Western blot (confirmatory)
HIV treatment & Prevention
Prevention
A- condom
B- pre-exposure prophylaxis
C- voluntary medical male circumsicion
Treatment
HAART- Highly Active AntiRetroviral Therapy
Carcinogenesis
A multistep process
Usually develop slowly over a long peeiod of time
Involve actuvation of multiple cellular oncogenes & inactivation of tumor suppressor Genes
VIRAL CARCINOGENESIS
◦ Viruses can cause cancer.
◦ Tumor viruses establish persistent infections.
◦ Host factors are important determinants of virus tumorigenesis.
◦ Viruses are seldom complete carcinogens.
◦ Virus infections are more common than virus-induced tumors.
◦ There are long latent periods between infection and tumor appearance.
◦ Viral strains differ in oncogenic potential.
◦ Viruses may be direct- or indirect-acting carcinogens.
◦ Direct-acting – introduction of transforming genes; highly oncogenic
◦ Indirect-acting – alteration of the expression of pre-existing cellular genes; weakly
oncogenic
◦ Cancer viruses modulate growth pathways.
◦ Viral markers are present in tumor cells.
◦ Integration and retention of viral nucleic acid in host cell (DNA viruses and retroviruses).
◦ One virus may cause more than one type of tumor.
Oncogenes
◦ mutated derivatives of normal genes
(proto-oncogenes) whose protein products
act to accelerate cell growth or cell division
◦ mutation of a proto-oncogene increases
the activity or amount of the gene product
(gain of function), thereby increasing cell
proliferation
◦ requires only 1 allele to be mutated
◦ occurs only in somatic cells (cannot be
inherited)
◦ RNAViruses
Tumor SuppressorGenes
◦ produce protein products that normally
suppress cell growth or cell division,
promote cell death or repair DNA
◦ mutation in tumor suppressor genes
deccreases the activity or amount of the
gene product (loss of function), thereby
increasing cell proliferation
◦ requires both alleles to be mutated
◦ occurs in somatic and germ cells (can be
inherited)
◦ DNAViruses
ONCOGENIC VIRUSES
◦ DNA Viruses
◦ Papillomaviridae
◦ Polyomaviridae
◦ Adenoviridae
◦ Herpesviridae
◦ Hepadnaviridae
◦ Poxviridae
◦ RNA Viruses
◦ Retroviridae
◦ Flaviviridae
