VIRUS TRANSMISSIO PATHOGENESIS & CLINICAL FEATURES DIAGNOSIS TREATMENT PREVENTION

N IMMUNITY
HIV -Natural host: CD4+ Helper T cell- Three stages -ELISA – --No vaccine available
Retrovirus man. Free HIV necrosis – suppression Early acute stage:: Normal antibodies -AZT --HIV mutates too rapidly
-Human T cell or HIV infected of CMI – opportunistic CD4 cell count 1200mm3 -Western Blot (Azidothymidine) --Reverse Transcriptase
lymphotrophic cells by infections and tumors -Initial viremia - After 2-4 wks. analysis – causes at least 1
virus exposure to Kaposi sarcoma & Fever, headache, lethargy, antibodies Inhibits Reverse mutation each time it is
-Human infected body Lymphoma. Th17 cells muscle aches, sore throat, -Ora quick - Transcriptase used
immunodeficiency fluids. 4 Body killed – predispose to generalized lymphadenopathy, Rapid immuno -Avoid exposure to virus.
virus HIV –1 Fluids: Blood, blood borne infections -assay for -HAART Highly Active Needle sharing, discard
maculopapular rash on trunk,
-Human Semen, Vaginal Genital tract mucosal antibody Antiretrovial Therapy contaminated blood,
arms, leg ( sparing palm &
immunodeficiency Secretions, dendritic cell soles). Leukopenia. -Culture condom
two nucleoside
virus HIV –2 mothers Milk. (langerhans) → CD4+ -Resolve in 2 wks. Patient -PCR – qualitative -Post exposure
inhibitors (Zidovudine,
-Sub group Risk increased cells infected. HIV infective, antibodies , prophylaxis – HAART
Lamivudine)
Lntivirus in STDs found in blood after 4- detectable after 3-4 wks. quantitative regimen
Envelope: Type 1. High Risk 11 days of infection -Viral set point amount of virus -Prefer LSCS instead of
one protease inhibitor
secific antigen unprotected Brain – monocytes, i.e. Viral load occur, tend to vaginal delivery
(Indinavir)
glcoprotein Sexual Contact macrophages → giant remain set over years. Higher -Avoid lactation
1. gp120 2. Needles cells – cell death in set point – progression. Viral -Acute infection
2. gp41. Needle pricks syncitia → immune load guides treatment
Sub types A-I. and dental attack by CD8+ cells → decisions. More than .2 reverse
Antibody procedures CNS effects 10,000copies/ ml plasma transcryptase
neutralizes Intravenous HIV -super antigen → SYMPTOMS inhibitors (efavirenz)
infection Drug Abuse activation of many 1)SYSTEMIC:
-Nucleocapsid: p24 (sharing dirty helper T cells → fever,weight loss .one protease
gp specific antigen needles) death. Persistently 2)pharyngitis inhibitor (side effect –
seological marker, Accidental infected T cells – 3)mouth buffalo hump)
SS RNA, diploid i.e. needle sticks continued HIV Sores , thrush
2 identical copies, 3. Blood to production. Persistent 4)muscles -Enfuvirtide fusion
Br shaped, + Blood Contact infection, even Life Myalgia inhibitor. New
plarity Open sores or long. Latent infection 5)liver and spleen
wounds, in CD4+ cells and Enlagrment -Drugs to prevent
Transfusions, immature thymocytes 6)central opportunistic
Organ serve as continuous Malaise, headache, infections
Transplants, source of virus neuropathy
Artificial Evasion of immune 7)lymph nodes -Drug resistant
Insemination system Lymphadenopathy mutants emerged
4. Mother to -Escape mutants, 8)Skin
Child mutaton in class I Rash
Placenta, MHC –failure of HIV 9)gastric
Passage of epitoe presentation to Nausea,vomiting
baby through cytotxic T cells – Middle latent stage
birth canal, unchcked proliferation CD4 cell count < 1000mm3
Breast milk of virus -Low viremia. Sequestered HIV
Saliva, tears -Integration in host in lymph nodes “latent” inside
seem to play cell DNA CD4 cells. Median latency
no role -High mutation rate period - 10 yrs.
env genes for gp120 -HIV Positive - antibodies
-Tat and nef pr- Down detected in blood
regultion of class I pr -Seroconversion
Elite controllers 6 to 8 weeks
-Rare group of HIV -Syndrome - AIDS Related
infeced people who Complex (ARC). Persistent
have no detectable fever, fatigue, wt loss,
HIV in their blood with lymphadenopathy
norml CD4+ cell count. Late stage / symptomatic
Mecanism unclear. immunodeficiency:
Certain HLA alleles are -CD4+ cell ≤400- 600/uL
protetive, an inhibitor -Viral Genome “turned on”,
of cyclin dependant Symptoms begin to appear
kinase p21 plays role Factors that turn the genome
Other Non on
progressors -Other infections (Herpes
-Have mutations in nef Simplex 1, Syphilis)
genes -Stress or shock to the system
Production of large -Alcohol, drug abuse
amounts of ɑ -nutrition
defensins -Exercise (Lack of or too
much?)
-Sunburn ?
-Once HIV Genome is “turned
on” death usually results
within 2 years
Symptoms
-chronic fatigue, low-grade
fever, night sweats,
-Diarrhea, weight loss
Opportunistic Bacterial,
Fungal and Viral Infections
-Pneumocysitis carinii
pneumonia (PCP)
-Fungal infections (thrush,
vaginal, disseminated
Histoplasmosis, cyptococcal
meningitis
-Tuberculosis, Viral ( CMV,
herpes)
-Toxoplasmosis (Brain)
Protozoal
Neurological - Dementia ,
Neuropathy
Kaposi’s Sarcoma ( Cancer -
Skin and Blood vessels)
Advanced Disease
(AIDS)CD4 cell count <
200mm3