Micro/simple

Front 1

What are the 4 HIV related CD4 T cell differentiations?

Back 1

1. Normal CD4+ T-cell counts are 1000 cells/microlit/blood.
In HIV infected persons the count declines by about 60 cells/mlblood/year.
2. CD4+ T cell count of 400-200(about 7 years). Constitutional symptoms, weight loss fever night sweats adenopathy with skin infections, Candida and herpes zoster. Tbc may be more common as well.
3. CD4+ T cell count less than 200(8 years)Very serious opportunistic infections set in. Pneumocystis carinii, Cryptococcus and Toxoplasma.
4. CD4+ T cell count less than 50. Immune system is compromised almost fully. M. avain intracellulare causes disseminated disease. Cytomegalovirus infections increase.

Front 2

How is viral load assessed in HIV?

Back 2

CD4 counts are used to detwrmine severity of disease. measurement is via PCR or branched chain DNA assay.

Front 3

What is the mechanism of T cell death?

Back 3

The CD4 receptor appears to be involved in T cell death. Monocytes and macrophages which have fewer CD4 receptor concentrations, are not destroyed as extensively as T cells.
There are 3 mechanisms of T cell death.

Front 4

What is the 1st phase of T cell death/

Back 4

When the virion is budding, the gp160, in the T cell membrane may bind to adjacent CD4 receptors on the same T helper cell membrane, lacerating the T cell membrane.

Front 5

What is the 2nd phase of T cell destruction?

Back 5

A second phenomenon occurs between infected cells and non-infected Cd4 cells. The gp160 in the infected cells bind to other CD4 T helper cells, resulting in cell to cell fusion, forming multinucleated giant cells.

Front 6

What is the third potential mechanism of T cell death?

Back 6

Gp160 in the T cell membrane may mark the cell as non self, resulting in auto immune T cell destruction by cytotoxic CD8 T lymphocytes.

Front 7

A healthy person has about 1000 CD4+ T helper cells per ml/blood. TRUE/FALSE

Back 7

TRUE.

Front 8

What is the advantage of creating multinucleated giant cells?

Back 8

It allows the virus to pass from an infected cell to an uninfected cell, without contacting the blood. This also protects it from circulating antibodies.

Front 9

Does B cell dysfunction occur in HIV?

Back 9

Yes. There is a polyclonal activation of B cells resulting in an outpouring of immunoglobulins. This hypergammaglobinemia results in immune complex formation and autoantibody formation. There is a decreased abilty to produce antibodies in response to new antigens.

Front 10

Hiv infects monocytes and macrophages and actively divides within them. TRUE/FALSE

Back 10

TRUE. These cells serve as reservoirs, and they migrtae across the blood brain barrier carrying HIV to the CNS.

Front 11

AIDS patients suffer from a high incidence of B cell lymphoma often presenting with a brain mass. TRUE/FALSE

Back 11

TRUE. Infact half of these lymphomas have Epstein-Barr virus DNA.

Front 12

regarding Kaposi's sarcoma, 96% of these cases are seen in homosexual men. TRUE/FALSE

Back 12

TRUE. There may be a cofactor which appears to be a new herpes virus called HHv-8. Its DNA sequences have been found in Kaposi's sarcoma and antibodies to HHV-8 are found as well.
lesions are red to purple plaques or nodules and arise on the skin all over the body.

Front 13

Aids patients often have many permanent indwelling catheters. These serve as entry points for bacteremia caused by Staph. aureus or Staph epidermidis. TRUE/FALSE

Back 13

TRUE.
Infact tbc and Mycobacterium avium intracellulare(MAI) are seen. This latter disease is very rarely seen in non HIV patients.

Front 14

List 3 HIV related fungal infections commonly seen?

Back 14

1. Candida albicans-it causes oral thrush and esophagitis.
2. Cryptococcus neoformans- causes meningitis in 10% of AIDS patients. A normal host with meningitis would have meningeal inflammation with meningismus(positive Kernig's and Brudzinski's sign) stiff neck and headache. CSF testing can confirm this.
3. Histoplasma capsulatum/Coccidioides immitis(lungs, skin and other areas).

Front 15

What are some co-viral infections seen in AIDS patients?

Back 15

1. Herpes zoster-painful skin vesicles.
2. Epstaein Barr virus- may cause "oral hairy leukoplakia(OHL). This can occur in CD4 counts <400 and is given by white hairlike projections arising from the side of the tongue.
3. Herpes simplex
4. Cytomegalovirus(CMV)- may cause blindness and chorioretinitis.

Front 16

List 2 protozoal infections of HIV.

Back 16

1. Pneumocystis carinii pneumonia(PCP) This is a common opportunistic infection. 80% of AIDS patients will get this atleast once in their lifetime unless prophylactic antibiotics are given.
2. Toxoplasma gondii- will cause mass lesions in the brain with seizures, weakness and aphasia.
3, Cryptosporidium/Microsporidia and Isospora-these parasites can cause chronic diarrhea.

Front 17

How is the diagnosis of HIV and AIDS acheived?

Back 17

Following infection with HIV, viral antigens(p24) can be detected in the blood within weeks. Six weeks later antibodies appear.
Elisa/western blot.

Front 18

What is the Western Blot test?

Back 18

In this test, HIV antigens(gag, pol and env) are separated in bands on paper by molecular weight. patients serum is added to this paper. if the serum has antibodies against HIV antigens they will stick to the antigens on the paper.
lastly anti-human antibodies(labeled with enzymes) are added, these stick to the antibodies on the antigens lighting up bands on the paper. This test is considered positive if it has bands to 2 HIV gene products(p24, gp41 and gp120).

Front 19

Regarding, control treatment and Cure, list 4 approaches.

Back 19

1. prevention of HIV infection
2. Vaccine development
3. Limiting growth of HIV, once it has occurred.
4. Treating opportunistic infections that can cause death.
prevention involves blood screening, education and risky behavior.

Front 20

Regarding vaccine development, what is a V3 loop?

Back 20

Persons infected with HIV develop antibodies against HIV determinants. Early in HIV infection antibodies arise that bind to a hypervariable portion of the envelop glycoprotein gp120 called the V3 loop. These V3 specific antibodies will neutralize only the exact starin of HIV, that elicited the antibody.

Front 21

What are some challenges to the development of a successful vaccine?

Back 21

1. Rapid mutation- HIV envelop glycoproteins mutate rapidly, so there are mant starins. The rapidly mutating V3 loop of gp120 and the reverse transcriptase enzyme combined with rapid viral reproduction over a long disease course results in different quasi-species, even in the same individual.
2. HIV is transmitted from cell to cell(syncytial formation).
3. Poor animal model- Apes cannot infected with HIV, but they can with SIV. Animal models are costly, and the ethical ramifications are often an obstacle.

Front 22

What are some of the latest vaccine research efforts?

Back 22

1. Live viruses-risky
2. Recombinent HIV-1 envelop glycoprotein vaccine can be made by splicing the HIV gene. This woulkd protect only against the exactly used antigen.
3. Live recombinent organisms
4. Direct IM vaccines
5. Soluble CD4 receptors. These bind to HIV gp120 thus preventing HIV from binding to the CD4+T helper cell. This has proved valuable in the SIV virus.

Front 23

How is Pneumocystis carinii pneumomia treated?

Back 23

Trimethoprim and Sulfamethoxazole given prophylactically when CD4+ T cell counts drop below 200-250.

Front 24

How is Toxoplasam gondii treated?

Back 24

Brain lesions are treated with tetrahydrofolate reductase inhibitor/sulfa combination called pyramethamine/sulfadiazine.

Front 25

How is M. avian intracellulare?

Back 25

Azithromycin or Clarithromycin.
herpes varicella zoster-acyclovir
candida albicans-oral clotrimazole, nystatin or fluconazole.