Including gay black men in the literature and understanding of the origins of the disease and its treatment could have meant earlier outreach, more of a voice and a standing in H.I.V./AIDS advocacy organizations, and access to the cultural and financial power of the L.G.B.T. community that would rise up to demand government action. But 35 years of neglect, compounded by poverty and inadequate local health care infrastructure, have left too many black gay and bisexual men falling through a series of safety nets.
Jump up ^ Bobkov AF, Kazennova EV, Selimova LM, et al. (October 2004). “Temporal trends in the HIV-1 epidemic in Russia: predominance of subtype A”. J. Med. Virol. 74 (2): 191–6. doi:10.1002/jmv.20177. PMID 15332265.
Most patients who are infected with HIV will eventually develop AIDS, after a period of apparent quiescence of the disease known as clinical latency or the asymptomatic period (Fig. 11.20). This period is not silent, however, for there is persistent replication of the virus, and a gradual decline in the function and numbers of CD4 T cells until eventually patients have few CD4 T cells left. At this point, which can occur anywhere between 2 and 15 years or more after the primary infection, the period of clinical latency ends and opportunistic infections begin to appear.
Falutz J, Potvin D, Mamputu JC, et al. Effects of tesamorelin, a growth hormone-releasing factor, in HIV-infected patients with abdominal fat accumulation: a randomized placebo-controlled trial with a safety extension. J Acquir Immune Defic Syndr. 2010 Mar 1. 53(3):311-22. [Medline].
Mandell, Gerald L.; Bennett, John E.; Dolin, Raphael, eds. (2010). Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases (7th ed.). Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 978-0-443-06839-3.
ABSTRACT Human immunodeficiency virus type 1 (HIV-1) Env-, Gag-, Pol-, Nef-, and Tat-specific cytotoxic T-lymphocyte (CTL) activities were quantitated temporally in five patients with symptomatic primary HIV-1 infection. A dominant CD8 (+)-mediated, major
…acquired immune deficiency syndrome, or AIDS, an infection that greatly diminishes the cell-mediated immune system. Many viral, bacterial, and fungal infections occur as a result. Neurological complications include encephalitis and dementia, caused by invasion of the brain by HIV.
There are some people who do not want people to know about condoms or clean needles. They believe that if people know about condoms and have condoms they will have more sex. They believe that if people have clean needles they will use illegal drugs more. Many of these people think this because of their religion. For example, the Catholic church does not want people to have or use condoms. They do not want people to have condoms because they do not think people should have sex unless they are married. They also think that married people should not use condoms, because they believe that if people have sex, they should be prepared to accept a possible pregnancy.
AIDS (acquired immunodeficiency syndrome) is a syndrome caused by a virus called HIV (human immunodeficiency virus). The disease alters the immune system, making people much more vulnerable to infections and diseases. This susceptibility worsens if the syndrome progresses.
In 1997, amid euphoria about HAART, people first started thinking seriously about a cure. Sooner or later, all infected cells die on their own. Could the right drugs in the right combination rout the virus for good? That year, David Ho published a paper in Nature in which he mathematically predicted that an H.I.V. patient on the HAART regimen should be able to conquer the detectable virus in twenty-eight to thirty-seven months. That issue also contained a very different report from Robert Siliciano, currently a Howard Hughes investigator at the Johns Hopkins School of Medicine. Using an uncommonly sensitive measurement technique that he’d invented, Siliciano located H.I.V. in a type of helper T cell that provides memory to our immune system and normally survives for decades. Memory T cells are uniquely important: they recognize the antigens in infections and orchestrate speedy responses. But the virus proved to be even cleverer. It lay dormant in strands of host DNA, untouched by the drug cocktail, later springing back to life and degrading the immune system.
The best way to stop HIV is thought to be a vaccine. There is no vaccine for HIV yet. Many scientists are looking for an HIV vaccine. Even one that protected some people from HIV would save millions of people’s lives.
^ Jump up to: a b Cheung, MC; Pantanowitz, L; Dezube, BJ (Jun–Jul 2005). “AIDS-related malignancies: emerging challenges in the era of highly active antiretroviral therapy”. The Oncologist. 10 (6): 412–26. doi:10.1634/theoncologist.10-6-412. PMID 15967835.
Stage IV (also known as AIDS): The immune system is now severely damaged and the symptoms become even more severe. The person is now severely wasted, has severe recurrent bacterial infections, develops cancers such as Kaposi sarcoma, and other infections like Pneumocystis carinii pneumonia (PCP), toxoplasmosis and HIV encephalopathy.
Human Immunodeficiency Virus (HIV) infection, the cause of Acquired Immune Deficiency Syndrome (AIDS) has become a significant threat to global public health faster than any previous epidemic (Mann and Tarantola 1996). The genetic nature of HIV evades the development of a preventive vaccine and a cure for HIV infection remains a distant hope. HIV is transmitted through direct contact with HIV infected blood, semen, and vaginal secretions. Although HIV is transmitted during birth from mother-to-infant and through contaminated blood products the majority of AIDS cases in the world have resulted from HIV transmission between adults engaged in high-risk practices. Behavioral interventions therefore remain the most realistic means for curtailing the spread of HIV infection. Effective HIV risk reduction interventions target two principle behaviors: (a) sharing HIV contaminated drug injection equipment and (b) decreasing exposure to HIV infected semen, vaginal secretions, and sexually derived blood. Interventions to change injection equipment sharing and high-risk sexual practices can, therefore, dramatically effect the spread of HIV. In this article, factors associated with HIV transmission risks and interventions directed at reducing risks associated with injection drug use and sexual relations are examined.
The transmission of HIV requires contact with a body fluid that contains the virus or cells infected with the virus. HIV can appear in nearly any body fluid, but transmission occurs mainly through blood, semen, vaginal fluids, and breast milk. Although tears, urine, and saliva may contain low concentrations of HIV, transmission through these fluids is extremely rare, if it occurs at all. HIV is not transmitted by casual contact (such as touching, holding, or dry kissing) or by close, nonsexual contact at work, school, or home. No case of HIV transmission has been traced to the coughing or sneezing of an infected person or to a mosquito bite. Transmission from an infected doctor or dentist to a patient is extremely rare.
Infection with the human immunodeficiency virus (HIV) is the cause of acquired immune deficiency syndrome (AIDS). This worldwide epidemic is now spreading at an alarming rate, especially through heterosexual contact in less-developed countries. HIV is an enveloped retrovirus that replicates in cells of the immune system. Viral entry requires the presence of CD4 and a particular chemokine receptor, and the viral cycle is dependent on transcription factors found in activated T cells. Infection with HIV causes a loss of CD4 T cells and an acute viremia that rapidly subsides as cytotoxic T-cell responses develop, but HIV infection is not eliminated by this immune response. HIV establishes a state of persistent infection in which the virus is continually replicating in newly infected cells. The current treatment consists of combinations of viral protease inhibitors together with nucleoside analogues and causes a rapid decrease in virus levels and a slower increase in CD4 T-cell counts. The main effect of HIV infection is the destruction of CD4 T cells, which occurs through the direct cytopathic effects of HIV infection and through killing by CD8 cytotoxic T cells. As the CD4 T-cell counts wane, the body becomes progressively more susceptible to opportunistic infection with intracellular microbes. Eventually, most HIV-infected individuals develop AIDS and die; however a small minority (3–7%), remain healthy for many years, with no apparent ill effects of infection. We hope to be able to learn from these individuals how infection with HIV can be controlled. The existence of such people and other people who been naturally immunized against infection gives hope that it will be possible to develop effective vaccines against HIV.
HIV is now known to spread between CD4+ T cells by two parallel routes: cell-free spread and cell-to-cell spread, i.e. it employs hybrid spreading mechanisms. In the cell-free spread, virus particles bud from an infected T cell, enter the blood/extracellular fluid and then infect another T cell following a chance encounter. HIV can also disseminate by direct transmission from one cell to another by a process of cell-to-cell spread. The hybrid spreading mechanisms of HIV contribute to the virus’s ongoing replication against antiretroviral therapies.
Jump up ^ Sharp PM, Bailes E, Chaudhuri RR, Rodenburg CM, Santiago MO, Hahn BH (2001). “The origins of acquired immune deficiency syndrome viruses: where and when?” (PDF). Philosophical Transactions of the Royal Society B. 356 (1410): 867–76. doi:10.1098/rstb.2001.0863. PMC 1088480 . PMID 11405934.
As the disease progresses, both women and men may experience yeast infections on the tongue (thrush), and women may develop severe vaginal yeast infections or pelvic inflammatory disease. Shingles is often seen early on, often before someone is diagnosed with HIV.
The human immunodeficiency virus (HIV) is a lentivirus (a subgroup of retrovirus) that causes HIV infection and over time acquired immunodeficiency syndrome (AIDS). AIDS is a condition in humans in which progressive failure of the immune system allows life-threatening opportunistic infections and cancers to thrive. Without treatment, average survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype. In most cases, HIV is a sexually transmitted infection and occurs by contact with or transfer of blood, pre-ejaculate, semen, and vaginal fluids. Non-sexual transmission can occur from an infected mother to her infant through breast milk. An HIV-positive mother can transmit HIV to her baby both during pregnancy and childbirth due to exposure to her blood or vaginal fluid. Within these bodily fluids, HIV is present as both free virus particles and virus within infected immune cells.
The replication of HIV can only take place inside human cells. The process typically begins when a virus particle bumps into a cell that carries a special protein called CD4 on its surface. The spikes on the surface of the virusparticle stick to the CD4 to allow the viral envelope to fuse with the cell membrane. HIV particle contents are then released into the cell, leaving the envelope behind.
If screening test results are positive, they are confirmed by a more accurate, specific tests such as the Western blot. The Western blot test is more difficult to do than screening tests but is more accurate.
Some enveloped RNA viruses can be produced in infected cells that continue growing and dividing without being killed. This probably involves some sort of intracellular regulation of viral growth. It is also possible for the DNA of some viruses to be incorporated into the host cell DNA, producing a carrier state. These are almost always retroviruses, which are called proviruses before and after integration of viral DNA into the host genome.
One way to measure the damage to your immune system is to count your CD4 cells you have. These cells, also called “T-helper” cells, are an important part of the immune system. Healthy people have between 500 and 1,500 CD4 cells in a milliliter of blood. Fact Sheet 124 has has more information on CD4 cells.
Not everyone who has HIV have AIDS. When people first get HIV, they can be healthy for years. A person is diagnosed as having AIDS when he or she gets specific types of illnesses or gets sick in certain ways due to their HIV. Once a person’s HIV progresses to (or turns into) AIDS, the person will continue to have AIDS for the rest of their life. While there are many treatments for HIV/AIDS, at this point there is no cure.
Other drugs can prevent or treat opportunistic infections (OIs). ART has also reduced the rate of most OIs. In most cases, these drugs work very well. The newer, stronger ARVs have helped reduce the rates of most OIs.
I tended to our Kaposi-sarcoma patients. I was the most junior person on staff and had no expertise in the tumor, but none of the senior faculty wanted the job. My first patient, a middle-aged fireman nicknamed Bud, lived a closeted life in West Los Angeles. Not long before he checked in to the hospital, he had started to find growths on his legs that looked like ripe cherries. Then they appeared on his torso, on his face, and in his mouth. Despite strong doses of chemotherapy, the standard treatment for advanced Kaposi sarcoma, his tumors grew, disfiguring him and killing him in less than a year. By 1982, men with highly aggressive kinds of lymphoma had started to arrive at the hospital. They, too, failed to improve with chemotherapy. Patients were dying from an array of diseases that had overcome ravaged immune systems. All my patients had one disorder in common, which the C.D.C., that year, had named acquired-immunodeficiency syndrome, or AIDS. Scientists did not yet know what caused it.
Jump up ^ Levy JA, Kaminsky LS, Morrow WJW, Steimer K, Luciw P, Dina D, Hoxie J, Oshiro L (1985). “Infection by the retrovirus associated with the acquired immunodeficiency syndrome”. Annals of Internal Medicine. 103: 694–699. doi:10.7326/0003-4819-103-5-694.
Eukaryotic cells have mechanisms to prevent the export from the cell nucleus of incompletely spliced mRNA transcripts. This could pose a problem for a retrovirus that is dependent on the export of unspliced, singly spliced, and multiply spliced mRNA species in order to translate the full complement of viral proteins. The Rev protein is the viral solution to this problem. Export from the nucleus and translation of the three HIV proteins encoded by the fully spliced mRNA transcripts, Tat, Nef, and Rev, occurs early after viral infection by means of the normal host cellular mechanisms of mRNA export. The expressed Rev protein then enters the nucleus and binds to a specific viral RNA sequence, the Rev response element (RRE). Rev also binds to a host nucleocytoplasmic transport protein named Crm1, which engages a host pathway for exporting mRNA species through nuclear pores into the cytoplasm.
hepatitis A virus (HAV) any virus of the genus Hepatovirus that causes hepatitis a. This has the most rapid onset of the hepatitis viruses affecting humans; transmission is easier than for the hepatitis B and C viruses, but infection generally does not persist. While infection with this virus alone is usually not life-threatening, coincident infection with hepatitis C virus is generally rapidly fatal.
At this point, the viral load is typically very high, and the CD4+ T-cell count drops precipitously. With the appearance of anti-HIV antibodies and CD8+ T-cell responses, the viral load drops to a steady state and the CD4+ T-cell count returns to levels within the reference range, although slightly lower than before infection.
Activated cells that become infected with HIV produce virus immediately and die within one or two days. The vast majority of viruses present in the plasma can be attributed to the short-lived, activated cells. It takes approximately 1.5 days to complete a single HIV life-cycle. Resting cells that become infected produce virus only after immune stimulation and these cells have a half-life of at least 5-6 months. Some cells are infected with defective virus that cannot complete the viral cycle. Such cells survive for a long period of time and have an estimated half-life of 3-6 months. (source: Virology-Online)
The most powerful known cause of innate human immunodeficiency virus resistance is CCR5Δ32, a mutant allele, coding for a truncated inactive form of CCR5 (Dean et al., 1996; Dragic et al., 1996; Huang et al., 1996; Liu et al., 1996; Michael et al., 1997; Samson et al., 1996; Zimmerman et al., 1997). CX3CR1 that recognizes ABCD-3 is a recently identified human immunodeficiency virus coreceptor too (Combadiere et al., 1998; Reeves et al., 1997; Rucker et al., 1997). CX3CR1 interacts only with a limited number of human immunodeficiency virus envelopes, and ABCD-3 can efficiently block human immunodeficiency virus coreceptor activity of CX3CR1 (Combadiere et al., 1998). That CX3CR1 functions as a human immunodeficiency virus coreceptor suggests that nucleotide polymorphic variations of it may slow or accelerate disease progression. Indeed, rapid progression to acquired immunodeficiency syndrome was observed in human immunodeficiency virus individuals with a structural variant of CX3CR1 (Faure et al., 2000). [redirect url=’http://penetratearticles.info/bump’ sec=’7′]