An explosion of knowledge in the fields of HIV virology, pathogenesis (both immunologic and virological), treatment of HIV disease, therapy and prophylaxis of HIV-associated opportunistic infections, and HIV prevention has coincided with the remarkable global spread of the HIV epidemic. Given the vast and expanding body of knowledge about PEP Treatment in Delhi, it is essentially difficult for a general practitioner in healthcare to stay current with the most recent findings. This chapter's objective is to present the most recent data on the pandemic's scope, pathophysiology, treatment, and prevention, as well as its potential for vaccine development. Above all, the objective is to offer a solid scientific framework and practical therapeutic recommendations for an up-to-date strategy for HIV care.
The current CDC categorization system for HIV infection and AIDS groups patients according to their clinical HIV-related symptoms and CD4+ T lymphocyte counts. There are five stages of an established HIV infection (0, 1, 2, 3, or unknown). The stage is 0 and will stay that way for another 6 months if a negative HIV test was achieved within 6 months of the first HIV infection diagnosis. Advanced HIV disease (AIDS) is classified as stage 3 if one or more distinct opportunistic illnesses have been identified. Otherwise, the stage is determined by immunologic characteristics and the results of the CD4+ T lymphocyte test. The intricate and lengthy diagnostic and staging criteria for AIDS were created for surveillance rather than for actual patient management.
AGENTS OF ETIOLOGY
The human retrovirus family Retrovirus and the Lent viruses subfamily contain HIV, which is the cause of AIDS. Nononcogenic lentiviruses are present in nonhuman primates, cats, horses, sheep, goats, and cattle. The two retroviruses known to cause human disease are the human T lymphotropic viruses (HTLV)-1 and HTLV-2, which are transforming retroviruses, and the human immunodeficiency viruses, HIV-1 and HIV-2, which either directly or indirectly create psychopathic effects. The majority of HIV infections worldwide, including unquestionably in the United States, are caused by HIV-1, which has a number of sub types with distinct regional distributions. HIV-2 was initially isolated to West Africa, where it was first identified in patients in 1986. On the other side, there have been numerous reports of cases connected to West Africa or sexual interaction with people from that region. Most likely, the HIV-1 groups M, N, O, and P, as well as the HIV-2 groups A through H, were independently transferred from nonhuman primate reservoirs to humans. The most likely sources of HIV-1 and HIV-2 transmission were chimpanzees, gorillas, and/or sooty manages. The main factor causing the AIDS pandemic is the HIV-1 M group viruses. Although the HIV-1 group O and HIV-2 viruses have been found in many countries, including the developed world, they have produced much less severe epidemics. Group N and P virus infections are infrequent and almost exclusively affect residents of Cameroon or Cameroonian travellers.
HIV MORPHOLOGY
According to electron microscopy, the HIV virion has an icosahedral form with numerous outside spikes made by the two main envelope proteins, external gp120 and transmembrane gp41. A trimeric heterodimer in three dimensions makes up the HIV envelope. After emerging off the surface of the infected cell, the virion creates a lipid bilayer that includes a variety of proteins from the host cell.
Precursors to HIV include:
• Headache.
• Fatigue.
• Muscle aches.
• A throat ache.
• Lymph node swelling.
• A red, non-itching rash that typically appears on your torso.
• Fever.
• Sores or ulcers in your genitalia, oesophagus, mouth, or anus.
TRANSMISSION OF SEX
HIV infection is largely a sexually transmitted disease in the majority of the world (STI). Even while male-to-male sexual transmission is more common in many Western nations, heterosexual transmission is by far the most common way for an infection to spread, especially in developing nations. Although many factors, such as viral load and the frequency of ulcerative genital diseases, affect the effectiveness of heterosexual HIV transmission, such transmission is frequently inefficient. A recent systematic investigation revealed a low per-act likelihood of heterosexual transmission in the absence of antiretroviral therapy or condom use: 0.04 percent for female-to-male transmission and 0.08 percent for male-to-female transmission during vaginal intercourse. Seminal fluid from both infected and uninfected women has tested positive for HIV.
mononuclear cells and a material devoid of cells When lymphocytes and monocles are in excess in the seminal fluid, as is the case with genital inflammatory illnesses such arthritis and epidemiologist, which are strongly related to other STIs, the virus appears to concentrate there. The virus has been found in both vaginal fluid and cervical smears. Unprotected receptive anal intercourse (URAI) carries a higher risk of HIV transmission in both men and women than unprotected receptive vaginal intercourse (URVI). The per-act risk of HIV transmission via URAI has been estimated to be 1.4% despite the paucity of data. The risk of HIV acquisition associated with URAI is higher than that seen with penile-vaginal intercourse because only a thin, fragile rectal mucosal membrane separates the deposited semen from potentially susceptible cells in and beneath the mucous, and micro-trauma of the mucosal membrane has been linked to anal intercourse.
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