Question | Answer |
---|---|
What type of virus is HIV-1 and where is it most common | HIV-1 is a retrovirus that causes AIDS most common in USA and most other parts of the world |
Is HIV an enveloped or naked virus | enveloped |
How is HIV-2 different from HIV-1 and where is it most commonly found | structurally similiar to HIV-1 but HIV-2 has a significantly different GENOME most commonly found in west africa and India. AIDS progresses slowly |
What is the surface glycoprotein gp120 on the surface of HIV used for | recognizes target cell allowing attachment to host cells |
What is the transmembrane protein gp41 in HIV used for | this is the protein that helps the virus penetrate cell to infect them |
What is the matrix protein p17 for | helps maintain the viral structure helps transport viral genome to host cell nucleus and assemble new virions |
what is Capsid antigen protein p24 for | encapsulates the genome, reverse transcriptase, protease, and integrase proteins |
What HIV viral genese are major targets for anti-HIV drugs | PR and RT |
about how many people world wide suffer from aids | 33.2million |
what percent of people suffering from HIV/AIDS are female | 50% |
HOw many new cases of aids are there each year | 2.5 million |
What racial/ethnic groups are highest group for new HIV or AIDS cases | Black and hispanic |
What is the annual risk of transmitting HIV of a person who doesn't know they are infected vs someone who knows they are infected | unknown annual risk of 6-10% chance of transmission Know annual risk of 1-2% chance of transmission |
Because the annual risk of transmission is so much lower for those who know they are infected what is the guideline from the CDC | that routine HIV testing be done from 13-64 years of ages unless patient specifically opts out |
What are the high risks for HIV | homosexual men, multiple partners, anal sex, traumatic sex, other STD present increase risk or transmission |
What are the principal cells infected by HIV | CD4 + T Cells and antigen present cells (APCs) but it can infect many different types of cells GI cells leads to chronic diarrhea and brain cells leads to lethargy and dementia |
What is the initial receptor that HIV recognizes on host cells and what viral receptor recognizes it | HIV initially recognizes the CD4 on host cells with its gp120 but also needs a coreceptor to allow entry of the virus |
What viral protein recognizes the coreceptor allowing for PENETRATION OF HOST CELL | gp41 recognizes coreceptor for CD4 it is cxcr4 and for macrophages it is ccr5 |
what is CXCR4 | the coreceptor that CD4 cells that HIV gp41 recognizes to allow penetration into the cell |
what is CCR5 | coreceptor on macrophages that HIV gp41 recognizes allowing penetration into host cell |
What is the difference for a TH cell getting infected with HIV and a macrophage getting infected with HIV | Th cell will be lysed to allow HIV virions to escape. Macrophage HIV virions are released over time and cell doesn't die |
Why is HIV genome highly variable | high error rate during reverse transcription |
What is ARS | acute retroviral syndrome that has symptoms of sore throat, fever, muscle and headaches, enlarged lymph nodes and a rash that disappear in 1-4 weeks |
Why do the symptoms of ARS clear up in 1-4 weeks | body can still replenish fresh CD4 cells and CTLs |
How does HIV infection typically manifest itself | as a slow progression as the body slowly looses ground until CD4+ cells fall below normal reaching low levels of around ~300cells/ul |
What are you most likely to see when HIV infection reaches point where CD4+ cell counts are ~300cells/ul | usually start to see malignant neoplasms such as kaposis sarcoma, lymphomas most B cell lymphomas, cervical and anal carcinoma and opportunistic infections such as fungi |
What is the deffinition of AIDS | patient that is HIV antibody positive and has CD4+ T cell count below 200/mm3 or less than 14% of total T cells have the disease |
What are the common protozoan opportunistic infections in AIDS | toxoplasmosis isospora belli infection cryptosporodiosis |
what are the common fungal opportunistic infections in AIDS | pneumocystosis cryptococcosis candidiasis histoplasmosis mycobacterial- TB, Myco Avium |
What are the common viral opportunistic infections in AIDS | persistent mucocutaneous herpes simplex cytomegalovirus varicella zoster multifocal leukoencephalopathy |
How do you dx HIV | demonstrate presence of HIV antibody by EIA testing or PCR detection fro viral RNA or DNA in the serum |
Would it be effective to test someone for aids using an EIA if they had an accidental needle stick the day before | no because it take about 4 weeks to develop antibodies that EIA is testing for |
which test would allow detection of HIV infection after recent exposure in the last 4 weeks PCR or EIA | PCR would be more reliable because EIA tests for antibodies that are generally not present in the first 4 weeks |
What is the confirmatory test for a positive EIA test for HIV | western blot test that uses antibodies specific to viral proteins |
What is the most effective way to stop the spread of HIV | education |
When should you begin treatment for HIV | as soon as infection is detected or accidental blood exposure to infected individual |
What does HAART stand for | highly active antiretroviral treatment |
What are the guidelines for starting HAART | symptomatic HIV infection or AIDS related condition regardless of CD4+ T cell count or CD4+ T cell count falls below 200/mm3 |
When should you consider starting HAART therapy | CD4+ T cell count is between 200 and 350/mm3 or HIV RNA is above 100,00 copies/ml |
What are the anti-HIV drugs in current use | NRTIs (nucleoside reverse transcriptase inhibitors) such as AZT, D4T, lamivudin, DDL and ddC -Non-nucleoside reverse transcriptase inhibitors -protease inhibitors |
Does HAART cure AIDS | no in controls viremia and increases CD4 cell counts discountinuing therapy can cause return of viremia and complications of AIDS |
What are fusion inhibitors in HIV therapy such as Enfuvirtide | interfer with HIV-1 entry into cell by inhibiting fusion of viral and cellular membranes by binding GP41 subunit on viral envelope |
In addition to antiviral treatment what should you also start for patients with T Cells below 200/mm3 | prophylaxis treatment for opportunistic infections such as P. Carinii or mycobacterium and other fungal infection |
Your CD4 T cell count is below 200 what would you wnat to start prophylaxis against | pneumocystis jiroveci |
When your T Cell count is below 50 what prophylaxis would you start | start prophylaxis against Mycobacterium avium complex |
What Prophylaxis treatment would you start with T cell count below 100 and positive anti toxoplasma IgG assay | prophylaxis against toxoplasmosis |
causitve agent of this tumor of blood and lymph vessels is herpesvirus HHV-8 | kaposi's sarcoma |
What 2 changes does HHV-8 cause in blood and lymph cells to cause the tumors to form | 1. the cells become spinle shaped and proliferate 2 extensive formation of new blood vessels occurs |
Which type of lymphoma is more common in HIV patients B cell lymphoma or T cell lymphoma | B Cell lymphoma |
What virus likely plays and indirect role in causing lymphomas in aids | Epstein Barr Virus EBV |
What is the oportunistic virus that causes cervical and anal carcinomas in aids patients | HPV types 16 & 18 |
What is Toxoplasma Gondii | obligate intracellular sporozoan causes toxoplasmosis |
What is the definitive host for toxoplasma gondii | GI Tract of Felines- CATS |
What type of cell does the parasite toxoplasma gondii infect and what problems can it cause | it infects macrophages and multiplies inside of them until they rupture. |
What is the problem with congenital toxoplasmosis | can cause abortion and stillbirth when infected mother passes parasite to unborn child |
If a child that gets congenital toxoplasmosis doesn't die in utero what other complication can they have from the parasitic infection | CNS and Visceral problmes such as microcephaly, hydrocephaly, convulsion, hepatitis, pneumonia |
What is the main s/sx of asymptomatic toxoplasmosis | lymphadenopathy |
what other s/sx can accompany the typical lymphadenopathy of toxoplasmosis | fever, sore throat, rash, hepatosplenomegaly, atypical lymphocytosis |
What percent of aids patients or immunosuppresed individuals develop toxoplasmosis encephalitis | 50% with 90% of cases being fatal |
How do you dx toxoplasmosis | serologic testing detecting IgG antibodies by indirect hemaglutination test or indirect fluorescence test |
How can you prevent toxoplasmosis | proper hand washing after handling uncooked meat, cooking meat properly, avoid cat feces, cats shouldn't be allowed to hunt birds, rodents or eat undercooked meat |
how do you treat toxoplasmosis | pyrimethamine and sulfonamides (doesn't treat cyst form) Pregnant women gets spriamycin or there is a new drug that treats cysts too called atovaquone |
What virus family does cytomegalovirus belong | herpesviridae family enveloped double stranded DNA virus |
What is characteristic cytologically of a cytomegalovirus infection | infected cells are 2 or more time larger than normal unifected cells |
What is it called when cytomegalovirus enters a non replicating non infectious form and why is this significant to aids patients | latent cytomegalovirus which can reactivate in immunosuppressed and AIDS patients |
What are some of the manifestations of cytomegalovirus infection in AIDS patients | pneumonia chorioretinitis gastroenteritis neurological disorders fever fatigue splenomegal lymphadenopathy |
How do you dx cytomegalovirus | Detect CMV cytopathology, antigen or DNA in infected tissue. Isolate virus from tissue or secretions, presence of IgM antibody |
What is the tx for CMV | Gancyclovir, Foscarnet, Cidofovir Especially Gancyclovir with immune globulin reduces high mortality of CMV pneumonia |
What vaccines are not advised for AIDS patients | oral poliomyelitis Oral Typhoid BCG (TB vaccine) Varicella Zoster vaccine Yellow Fever Vaccine |
What vaccines should AIDS patients get | MMR FLU HEP A HEP B |