What three virion enzymes does HIV carry?
Reverse transcriptase, Integrase, Protease
What is the structure of HIV?
nucleic acid in center, surrounding core protein, matrix protein, envelop, envelop proteins
How many regulator genes are in HIV and which two are essential for replication?
6 total- tat and rev are essential
What are accessory genes?
Genes that are not essential for replication
Steps of replication process
attachmet of CD4 molecule, entry, uncoating
reverse transcriptase- RNA genome to proviral DNA
transported to nucleus
integrase unites proviral DNA to host DNA
host cell RNA polymerase transcribes proviral DNA to mRNA
Transmission of HIV
primarily through sexual contact
also through blood transfussion /perinatal infection
Pathogenesis of HIV
infection occurs in genital mucosa
HIV infects and kills lymphocytes leading to loss of CMI which predisposes to opportunistic infection
What happens to the helper T cells during HIV?
HIV kills helper T cells and cytoxic T cells also kill the virus infected helper T cells
What happens when helper T cells are reduced?
AIDS is produced
What is the main immune resistance to HIV?
cytotoxic T cells which controls the infection for a long time
What does polyclonal activation of B cells result in?
high immunoglobulin level which may cause auto immune disease through thrombocytopenia
3 stages of HIV infection
1. acute stage
2. Latent stage
3. Late immuno deficiency stage
Describe acute stage of HIV
present 2-4 weeks: fever, lethargy, sore throat, generalized lymphadenopathy, rashes on trunk, arms and legs, leukopenia
resolves spontaneously in 2 weeks
Abs appear after 3 -4 weeks
Describe latent stage of HIV
set point occurs- new viral production- viral load will reamain constant for a number of years (asymptomatic period), fatigue and weight loss can occur- viruses present in lymph nodes
Describe Late immuno deficiency stage
Decline in number of CD4 cells- increase in severity and frequency of opportunistic infections- immuno compromised state
What is the screening test for HIV
ELISA- HIV abs present from the serum
envelop Abs rise gradually and stay high in the end
Confirmed by western blot test
Treatment of choice for HIV
ziduvidin and lamivudin and indinavir- all together called Highly active anti retroviral therapy
given for lifetime
NNRTI can also be given
Treatment for children with AIDS
2 nucleoside inhibitors and 1 non nucleoside inhibitor
treatment is life long
no vaccine available
Common opportunistic infections in AIDS patients
Pneumocystic caini, kaposis sarcoma
Viral opportunistic infection in AIDS patients
Herp simplex, vzv, CMV
Fungal opportunistic infections in AIDS patients
Candida (thrush), crypto, meningitis and histplasma capsulatum
Protozoal opportunistic infections in AIDS patients
Bacterial opportunistic infections in AIDS patients
What does integration of viral genome to host cell DNA result in?
Where does Hepatitis A virus (HAV) replicate?
Transmission of HAV?
fecal contamination of water
Who are the reservoirs of HAV?
children most affected, humans are the only reservoir
Pathogenesis of HAV
liver cells are infected causing cell necrosis- when infection clears, damage is repaired
all viral infections look the same
Is HAV common in US?
YES- 50-75% of adults have abs
Clinical features of HAV?
after two weeks of infection, fever, anorexia, nausea, comiting and jaundice- dark colored urine, pale feces
most cases resolve in 2-4 weeks
most infections are asymptomatic
Vaccine for HAV?
YES- IgG provides life long immunity
Treatment for HAV?
no antiviral drug- only prevention
Prevention of HAV
proper sewage disposal, hand washing after defecation
Other name for Hep B virus?
Dane particle/hepadna virus
Describe look of HBV
enveloped DNA virus, partially double stranded
What does the envelop of HBV virus contain?
HBsAG- protein called surface antigen
also known as Australian Ag
What is the capsid protein of HBV known as?
core Ag - HBcAg
Distribution of Hep B virus?
world wide distribution
most prevelant in South east Asia- incidence of hepatocellular carcinoma here
Pathogenesis of Hep B
infects liver cells and causes necrosis
cytoxic T cells kill viral infected liver
Is there a chronic carrier stage of Hep B?
YES- few DNA integrates to host cell DNA
What does Ag-Ab complexes in HBV patients lead to?
arthralgia, arthritis, urticaria immune complex glomerulonephritis
Percentage of HBV patients that become chronic carriers?
What will occur in carrier HBV patients?
high incidence of hepatocellular carcinoma
What happens to patients who recover from HBV?
HBsAb is responsible for this!
Clinical features of HBV patient
prevelant for 10-12 weeks- similar symptoms as in other hepatitis virus but more serious jaundice
chronic infection leads to cirrhosis of liver/cancer
Treatment of chronic HBV infection
Alpha interferon and lamivudine (reverse transcriptase)
Prevention of HBV infection
vaccine available- vaccine contains HBsAg alone
What is available for passive immunity of HBV
Hyper immunoglobulin (anti serum) containing HBsAb
Who is the reservoir for Hep C (HCV)?
Transmission of HCV?
blood transfussion, IV drug addicts
Where is HCV common?
Pathogenesis of HCV?
infects hepatocytes- strongly predisposes to hepatocellular carcinoma
alcoholism enhances risk leading to cirrhosis
Clinical features of HCV
same as in HBV but milder
jaundice features will also be there
arthralgia, vasculitis and purpura occurs due to immune complexes
How do you detect HCV?
lab diagnosis by ELISA
something that will show increase in liver enzymes
Treatment of HCV?
alpha interferon and ribavirin
pegylated interferon- long acting
Is there a vaccine for HCV?
NO- hyper immuno globulin
What is the arbo virus?
arthropod born viruses
What does Arbo virus cause?
eastern/western equine encephalitis
west nile virus