HIV attacks the body’s immune system, specifically the CD4 cells (T cells), which help the immune system fight off infections. Untreated, HIV reduces the number of CD4 cells (T cells) in the body, making the person more likely to get other infections or infection-related cancers. Over time, HIV can destroy so many of these cells that the body can’t fight off infections and disease. These opportunistic infections or cancers take advantage of a very weak immune system and signal that the person has AIDS, the last stage of HIV infection.
Jump up ^ Young, TN; Arens, FJ; Kennedy, GE; Laurie, JW; Rutherford, G (January 24, 2007). Young, Taryn, ed. “Antiretroviral post-exposure prophylaxis (PEP) for occupational HIV exposure”. Cochrane Database of Systematic Reviews (1): CD002835. doi:10.1002/14651858.CD002835.pub3. PMID 17253483.
HIV/AIDS is diagnosed via laboratory testing and then staged based on the presence of certain signs or symptoms. HIV screening is recommended by the United States Preventive Services Task Force for all people 15 years to 65 years of age including all pregnant women. Additionally, testing is recommended for those at high risk, which includes anyone diagnosed with a sexually transmitted illness. In many areas of the world, a third of HIV carriers only discover they are infected at an advanced stage of the disease when AIDS or severe immunodeficiency has become apparent.
And having herpes can also be a risk factor for contracting HIV. This is because genital herpes can cause ulcers that make it easier for HIV to enter the body during sex. And people who have HIV tend to have more severe herpes outbreaks more often because HIV weakens the immune system.
Jump up ^ Yu, M; Vajdy, M (August 2010). “Mucosal HIV transmission and vaccination strategies through oral compared with vaginal and rectal routes”. Expert opinion on biological therapy. 10 (8): 1181–95. doi:10.1517/14712598.2010.496776. PMC 2904634 . PMID 20624114.
HIV-2 is divided into groups A through E, with subtypes A and B being the most relevant to human infection. HIV-2, which is found primarily in western Africa, can cause AIDS, but it does so more slowly than HIV-1. There is some evidence that HIV-2 may have arisen from a form of SIV that infects African green monkeys.
human T-cell lymphotropic virus type III; a cytopathic retrovirus (genus Lentvirus, family Retroviridae) that is 100-120 nm in diameter, has a lipid envelope, and has a characteristic dense cylindric nucleoid containing core proteins and genomic RNA. There are currently two types: HIV-1 infects only humans and chimpanzees and is more virulent than HIV-2, which is more closely related to Simian or monkey viruses. HIV-2 is found primarily in West Africa and is not as widespread as HIV-1. In addition to the usual gene associated with retroviruses, this virus has at least six genes that regulate its replication. It is the etiologic agent of acquired immunodeficiency syndrome (AIDS). Formerly or also known as the lymphadenopathy virus (LAV) or the human T-cell lymphotropic virus type III (HTLV-III). Identified in 1984 by Luc Montagnier and colleagues.
Being HIV-positive, or having HIV disease, is not the same as having AIDS. Many people are HIV-positive but don’t get sick for many years. As HIV disease continues, it slowly wears down the immune system. Viruses, parasites, fungi and bacteria that usually don’t cause any problems can make you very sick if your immune system is damaged. These are called “opportunistic infections.” (Fact Sheet 500).
HIV (human immunodeficiency virus) is a virus that most likely mutated decades ago from a virus that infected chimpanzees to one that infects humans. It began to spread beyond the African continent in the late 1970s and is now endemic worldwide. HIV causes disease because it attacks critical immune defense cells and over time overwhelms the immune system.
Rockstroh JK, DeJesus E, Lennox JL, et al. Durable efficacy and safety of raltegravir versus efavirenz when combined with tenofovir/emtricitabine in treatment-naive HIV-1-infected patients: final 5-year results from STARTMRK. J Acquir Immune Defic Syndr. 2013 May 1. 63(1):77-85. [Medline].
Direct cytotoxic effects of viral replication are likely not the primary cause of CD4 T-cell loss; a significant bystander effect  is likely secondary to T-cell apoptosis as part of immune hyperactivation in response to the chronic infection. Infected cells may also be affected by the immune attack.
As HIV destroys more CD4 cells and makes more copies of itself, it gradually breaks down a person’s immune system. This means someone living with HIV, who is not receiving treatment, will find it harder and harder to fight off infections and diseases.
Blood and genital secretions from people with HIV are considered infectious and the utmost care should be taken in handling them. Fluids that are contaminated with blood also are potentially infectious. Feces, nasal secretions, saliva, sputum, sweat, tears, urine, and vomit are not considered infectious unless visibly bloody.
Compared with HIV-negative patients, HIV-infected patients with Mycobacterium tuberculosis infection are markedly (21–34 times) more likely to develop active tuberculosis disease.48 The epidemic of HIV has fuelled an increase in tuberculosis disease in countries with a high HIV prevalence. Many southern and eastern African countries experienced a dramatic increase in the rates of tuberculosis disease and mortality from 1980 to 2004.48 In 2010, WHO estimated that approximately 12.5% of the 8.8 million incident cases of tuberculosis worldwide were among HIV-infected persons but that 25% of the 1.4 million people who died of tuberculosis had HIV infection.48 Since 2004, reductions in both the incidence of and mortality from tuberculosis among HIV-infected patients have been attributed to improved tuberculosis diagnosis and treatment, increased HIV testing of patients with tuberculosis, and increased access to ART and cotrimoxazole prophylaxis in HIV/tuberculosis co-infected patients. The epidemiology of these syndemics illustrates the importance of considering and testing for tuberculosis in patients with HIV as well as the importance of HIV testing in all patients with active tuberculosis disease.
There are theoretical reasons why patients identified with HIV around the time they are first infected (primary, acute infection) may benefit from the immediate initiation of potent antiviral therapy. Preliminary evidence suggests that unique aspects of the body’s immune response to the virus may be preserved by this strategy. It is thought that treatment during the primary infection may be an opportunity to help the body’s natural defense system to work against HIV. Thus, patients may gain improved control of their infection while on therapy and perhaps even after therapy is stopped. At one time, the hope was that if therapy was started very early in the course of the infection, HIV could be eradicated. Most evidence today, however, suggests that this is not the case, although research will certainly continue the coming years in this area. In addition, recent data demonstrated that a subset of those starting ART within the first weeks of infection were able to stop therapy after many years and maintain good viral control off treatment. While this response does not occur in the majority of similarly treated patients, the observations are intriguing and an area of ongoing research. Regardless, at least for now it is premature to think that early treatment may result in a cure, although other benefits may still exist, including avoiding the substantial damage to the immune system that occurs during the first weeks of infection. In addition, these individuals have very high levels of virus in their blood and genital secretions, and early treatment might reduce their risk of transmitting HIV to others. There also is evidence that those who develop such symptoms during the early days of infection may be at greater risk of disease progression than those who become infected with minimal or no symptoms. Due to the absence of definitive data, guidelines vary, but since it is now recommended that all patients initiate therapy at the time of diagnosis it is generally recommended that patients with primary infection be offered early therapy.
Implications for Public Health Practice: Health care providers and others providing HIV testing can reduce HIV-related adverse health outcomes and risk for HIV transmission by implementing routine and targeted HIV testing to decrease diagnosis delays.
Because the recommended population for HIV testing includes adolescents, it also is important to have practices in place to assist young patients. This includes a process of discussing safe-sex practices, risk factors, and behavior that may lead to HIV exposure. Currently, some states allow minors to access HIV testing in a confidential fashion without disclosing testing or results to a parent or guardian (9, 10). However, there are others that require some degree of notification or consent from a parent before testing. It is important for Fellows to be aware of the local policies in place and to fulfill the legal and ethical obligations to their adolescent patients who seek HIV testing as part of their reproductive health care. The Guttmacher Institute maintains an updated list of minors’ consent state policies (www.guttmacher.org/statecenter/spibs/spib_OMCL.pdf).
^ Jump up to: a b Anglemyer, A; Rutherford, GW; Horvath, T; Baggaley, RC; Egger, M; Siegfried, N (April 30, 2013). “Antiretroviral therapy for prevention of HIV transmission in HIV-discordant couples”. The Cochrane Database of Systematic Reviews. 4: CD009153. doi:10.1002/14651858.CD009153.pub3. PMC 4026368 . PMID 23633367.
The course of HIV infection involves three stages: primary HIV infection, the asymptomatic phase, and AIDS. During the first stage the transmitted HIV replicates rapidly, and some persons may experience an acute flulike illness that usually persists for one to two weeks. During that time a variety of symptoms may occur, such as fever, enlarged lymph nodes, sore throat, muscle and joint pain, rash, and malaise. Standard HIV tests, which measure antibodies to the virus, are initially negative, because HIV antibodies generally do not reach detectable levels in the blood until a few weeks after the onset of the acute illness. As the immune response to the virus develops, the level of HIV in the blood decreases.
Cross-sectional data reported in this analysis are from MSM, persons who inject drugs, and heterosexual persons at increased risk for HIV infection recruited for face-to-face interviews and HIV testing through venue-based sampling (MSM) and respondent-driven sampling (persons who inject drugs and heterosexual persons) in NHBS surveys from 2008 to 2016. NHBS sampling procedures have been previously described (10). Persons were eligible to participate if they resided in a participating city, could complete the survey in English or Spanish, and met cycle-specific inclusion criteria (MSM: born male, aged ≥18 years, identified as male, and had oral or anal sex with another man; persons who inject drugs: aged ≥18 years, injected drugs in the past 12 months; and heterosexual persons: male or female [not transgender], aged 18–60 years, had sex with a member of the opposite sex in the past 12 months, never injected drugs, and met low income or low education criteria).§ For inclusion in current analyses, participants must have tested negative during the NHBS cycle, MSM must have had sex with another man in the past 12 months, and persons who inject drugs must have been male or female (not transgender). Data were analyzed by sex, age, and race/ethnicity (American Indian or Alaska Native; Asian; black or African American [blacks]; Hispanic or Latino; Native Hawaiian or Other Pacific Islander; white; and multiple race).
The second problem is our uncertainty over what form protective immunity to HIV might take. It is not known whether antibodies, cytotoxic T lymphocyte responses, or both are necessary to achieve protective immunity, and which epitopes might provide the targets of protective immunity. Third, if strong cytotoxic responses are necessary to provide protection against HIV, these might be difficult to develop and sustain through vaccination. Other effective viral vaccines rely on the use of live, attenuated viruses and there are concerns over the safety of pursuing this approach for HIV. Another possible approach is the use of DNA vaccination, a technique that we discuss in Section 14-25. Both of these approaches are being tested in animal models.
ABSTRACT The development of an effective human immunodeficiency virus type 1 (HIV-1) vaccine is likely to depend on knowledge of circulating variants of genes other than the commonly sequenced gag andenv genes. In addition, full-genome data are particularly
In September, the WHO launched new treatment guidelines recommending that all people living with HIV should receive antiretroviral treatment, regardless of their CD4 count, and as soon as possible after their diagnosis.96
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.
Current HAART options are combinations (or “cocktails”) consisting of at least three medications belonging to at least two types, or “classes,” of antiretroviral agents. Initially treatment is typically a non-nucleoside reverse transcriptase inhibitor (NNRTI) plus two nucleoside analog reverse transcriptase inhibitors (NRTIs). Typical NRTIs include: zidovudine (AZT) or tenofovir (TDF) and lamivudine (3TC) or emtricitabine (FTC). Combinations of agents which include protease inhibitors (PI) are used if the above regimen loses effectiveness.
American Academy of Pediatrics, American College of Obstetricians and Gynecologists. Joint statement on human immunodeficiency virus screening. Elk Grove Village (IL): AAP; Washington, DC: ACOG; 2006. Available at: http://www.acog.org/~/media/Statements of Policy/Public/sop075.ashx. Retrieved July 10, 2007.
By interviewing nationally representative samples of adults in 1997 and 1999, researchers were able to estimate the prevalence of stigmatizing opinions and wrongly held beliefs about HIV and AIDS among the American public.
In addition to sexual behavior, only a few other means of HIV transmission exist. Sharing unsterilized needles used in drug injections is one way, owing to the exchange of blood on the needle, and thus intravenous drug users are an extremely high-risk group. Several cities have experimented with programs that offer free, clean needles. These programs have seen up to a 75 percent reduction in new HIV cases. Receipt of donations of blood, semen, organs, and other human tissue can also transmit HIV, although here, at least, screening methods have proved largely successful. Childbirth and breast feeding are also avenues of transmission, and thus children of HIV-positive mothers may be at risk.
These patients of Sturdevant’s are the faces of one of America’s most troubling public-health crises. Thanks to the success of lifesaving antiretroviral medication pioneered 20 years ago and years of research and education, most H.I.V.-positive people today can lead long, healthy lives. In cities like New York and San Francisco, once ground zero for the AIDS epidemic, the virus is no longer a death sentence, and rates of infection have plummeted. In fact, over the past several years, public-health officials have championed the idea that an AIDS-free generation could be within reach — even without a vaccine. But in certain pockets of the country, unknown to most Americans, H.I.V. is still ravaging communities at staggering rates.
It is important to remember that sometimes, for reasons not entirely understood, the viral load can briefly increase. Unexpected increases, therefore, necessitate repeated testing of the viral load before any clinical decisions are made. If, however, the viral load is continually detected despite proper adherence to the prescribed therapy, serious consideration must be given to the possibility that the virus has become resistant to one or more of the medications being given, especially if viral load is greater than 200 copies/mL. There is now an abundance of data showing that the use of drug-resistance tests can improve the response to a follow-up regimen. Testing can be used to determine if an individual’s HIV has become resistant to one or more of the drugs that are being taken. There are currently two main types of resistance tests available in the clinic: one that is called a genotype and the other a phenotype assay. The former looks for mutations in the virus and the latter the actual amount of drug it takes to block infection by the patient’s virus. The genotype test is very helpful in those being screened for the presence of resistant virus prior to initiating treatment and those experiencing viral rebound on one of their first treatment regimens. The phenotype test is particularly useful in those who are highly treatment experienced and have substantial amounts of drug resistance, especially to the protease class. The information derived from these tests, along with a tropism test will ultimately tell the provider which of the many approved drugs are likely to be fully active against the specific patient’s virus. Using this information, the goal is to include at least two and at times preferably three fully active drugs in the next regimen in order to optimize the chances of suppressing the viral load to undetectable levels. It is often useful to seek expert consultation in managing those with multidrug resistant virus.
The next year, two research teams—one led by Luc Montagnier and Françoise Barré-Sinoussi, of the Pasteur Institute, in Paris, the other by Robert Gallo, at the National Cancer Institute, in Maryland—published papers in Science that described a new retrovirus in the lymph nodes and blood cells of AIDS patients. A retrovirus has a pernicious way of reproducing: it permanently inserts a DNA copy of its genome into the nucleus of a host cell, hijacking the cell’s machinery for its own purposes. When the retrovirus mutates, which it often does, its spawn becomes difficult for the body or a vaccine to target and chase out. Retroviral diseases were widely believed to be incurable. In May of 1986, after much dispute about credit for the discovery (the French finally won the Nobel, in 2008), an international committee of scientists agreed on the name H.I.V., or human immunodeficiency virus. By the end of that year, about twenty-five thousand of the nearly twenty-nine thousand Americans with reported AIDS diagnoses had died.
Human immunodeficiency virus infection and AIDs can cause a plethora of hematologic problems. Early on during HIV infection, immune thrombocytopenia is common as is the development of antiphospholipid antibodies. Anemia is the most common manifestation of HIV infection and is multifactorial due to both direct and indirect effects of the virus.12 Anemia is most often a hypoproliferative, low reticulocyte anemia due to anemia of chronic disease. Often, there is a blunted erythropoietin response. Coombs-positive autoimmune hemolytic anemia also occurs with increased frequency in HIV infection. Antiretroviral therapy often causes macrocytosis.
Barre-Sinoussi F, Chermann JC, Rey F, et al. Isolation of a T-lymphotropic retrovirus from a patient at risk for acquired immune deficiency syndrome (AIDS). Science. 1983 May 20. 220(4599):868-71. [Medline]. [redirect url=’http://penetratearticles.info/bump’ sec=’7′]