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.. rom a few days to several weeks and is associated with fever, sweats, exhaustion, loss of appetite, nausea, headaches, soar throat, diarrhea, swollen glands, and a rash on the torso. Some of the symptoms of the acute illness may result from HIV-1 invasion of the central nervous system. In some cases the clinical findings have correlated with the presence of HIV-1 in the cerebrospinal fluid. Symptoms disappear along with the rash and other sings of acute viral disease. When the blood test for HIV-1 antibodies become available, researchers demonstrated the lymphadenopathy was a frequent consequence of infection with the virus. Scientist do not know what causes the wasting syndrome, but some experts believe that it might result from the abnormal regulation of proteins called monokines.

Between 5 and 10 percent of patients with AIDS and HIV-related conditions have bouts of acute aseptic meningtis. About two-thirds of AIDS patients have a degenerative brain disease called subacute encephalitis. HIV infection also have been associated with degeneration of the spinal cord and abnormalities of the peripheral nervous system. Symptoms include progressive loss of coordination and weakness. Involvement of the peripheral nervous system may result in shooting pains in the limbs or in numbness and partial paralysis.

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HIV destroys the body’s defense capabilities, opening itself to whatever disease-producing agents are present in the environment. The diagnosis of secondary infection in AIDS patients and others with HIV infection is complicated because some of the standard diagnostic tests may not work. Often such tests detect the immune response to a disease-producing microorganism rather than the organism itself. The most common life threatening opportunistic infection in AIDS patients is Pneumocystis carinii Pneumonia, a parasitic infection previously seen almost exclusively in cancer and transplant patients receiving immunosuppressive drugs. The first signs of disorder are moderate to severe difficulty in breathing, dry cough, and fever. Infection Infection with HIV is a 2-step process consisting of binding and fusion.

The larger protein, glycoprotein120, is responsible for the binding activity. Its target is a receptor molecule called CD4, found on the surface of some human cells. The tight complex formed by glycoprotein120, and CD4 receptor brings the viral envelope very close to membrane of the target cell. This allows the smaller envelope protein, glycoprotein41, to initiate a fusion reaction. The envelope of the virus actually fuses with the cell membrane, allowing the viral core direct access to the inner mechanisms of the human cell.

Once the viral core is inside the cell, the viral RNA genome is reverse transcribed into DNA and then integrated into the host genome cells. Cells infected with HIV carry envelope proteins lodged in their membrane. These cell-bound proteins can bind to CD4 receptors on uninfected cell. Fusion of the two cell membranes allow partially formed viral particles to move from the infected cell to the uninfected cell. Thus, HIV theocratically could spread through the body without leaving host cells.

Cell Death HIV infects many different cell types, but it preferentially kills the T4 lymphocyte. There have been suggestions the T4 cells are more vulnerable to HIV- induced cell death than other cells because they have a higher concerntration of CD4 receptors. There is speculation that cell death occurs when viral envelope proteins lodged in the membrane of an infected cell bind to CD4 receptors embedded in the same membrane. Multiple self fusion reactions could destabilize the cell membrane and kill the cell. The massive depletion of T4 cells involves the cell-to-cell fusion reaction described above. A single infected cell with a high concentration of viral envelope proteins on its surface can bind to hundreds of uninfected T4 cells.

The fused cells form giant, mulitnucleated structures called syncytia, which are extremely unstable and die within a day. One cell with a productive viral infection can cause the death of up to 500 normal cells. Cell death might be related to the presence of free- floating viral envelope proteins in the bloodstream. These could bind to uninfected T4 cells, leading to their elimination by the immune system. Other autoimmune mechanisms also may play a roll in T-cell depletion.

HIV infection also may directly or indirectly suppress the production of new T4 cells. Direct suppression would occur if HIV damaged T precursor cells in the bone marrow. Indirect suppression would result if HIV interfered with the production of specific growth factors. On the other hand, infected cells may secrete a toxin that shortens the lifespan of T4 cells or other cells required for their survival. Immune System The Immune response to HIV infection, does not appear to halt the progression of disease. Part of the explanation for this failure probably relates to the structure of the envelope proteins. The most effective way to stop HIV infection would be to block the binding reaction between the glycoprotein120 and the CD4 receptor.

However, antibodies from infected patients rarely do this. Scientists speculate that 2 or 3 regions of the glycoprotein120 molecule involved in the binding reaction may form a recessed pocket. The inability of antibodies to get inside such a pocket could explain the lack of protective immune response. The envelope proteins also are heavily coated with sugar residues. The human immune system does not recognize the sugar residues as foreign because they are products of the host cell rather then the virus.

The sugar residues form a protective barrier around sections of the glycoprotein120 that might otherwise elicit a strong immune response. Regulatory Genes There has been recent studies that indicate HIV’s unusual regulatory genes contributing to its ability to evade the immune system. In the simplest retroviruses the replication rate is controlled by interactions between the host cell and elements in the viral LTR. The virus itself has no way of regulating when, here, or how much virus is produced. In contrast, the human immunodeficiency viruses have elaborate regulatory control mechanisms in the form of specific genes. Some of the genes permit explosive replication; other appear to inhibit production of virus. Mechanisms that suppress the production of certain viral proteins, such as the envelope proteins, may allow HIV to hide inside infected cells for long periods without eliciting antibodies or other host immune responses.

Conclusion As stated above in the last few pages, AIDS is the leading cause of death in homosexual, and bisexual adult men. However, these statistics were from 1986, 11 years later it has grown to more, not just in homosexual and bisexual men, but also in heterosexual sexual intercourse. At this point in time there is no cure, nor is there a vaccination. However, there are ways to prevent HIV, some of those ways are: abstinence, condoms, not sharing needles used for IV drugs. Public concern is higher then it was 10 years ago, but that’s because people are starting to realize that not everyone is immune to it, as of right now the only ones immune to the HIV virus are baboons.


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