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Even just irritation of the genital areas can increase the risk, as it increases the number of cells that can serve as targets for Illustrations of hiv infection. Understanding how it is—and is not—transmitted is key for the success of control efforts. If a person is not ready to stop using drugs and is unable to purchase clean needles, many communities offer Illustrations of hiv infection programs. Apply for a Grant. People with circumcised penises are less likely to contract HIV from an HIV positive person during penis-vagina sex 1,4.
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Check out the animation on the TED Ed site. Each year, an additional 2 million people are newly infected with the virus. HIV infection can occur when an HIV virus reaches the mucosal membranes or the bloodstream of an individual. Helper T cells play a crucial role in defending the body against bacterial and fungal infections. Eventually, levels of the virus and helper T cells stabilize, and the infected individual experiences fewer symptoms.
Within a few months after the initial infection, viral loads are generally low and can remain at low levels for years, even without treatment. Over time, however, the amount of virus increases, and the levels of helper T cells decrease.
Other drugs prevent the virus from maturing, or block viral fusion, causing HIV to be unable to infect new cells in the body. Antiretroviral therapy is highly effective at managing the levels of HIV. Continued use has been shown to keep HIV-infected individuals from ever progressing to AIDS, and can lower the viral count to nearly undetectable levels. Unfortunately, antiretroviral therapy is not a cure for HIV.
Every so often, the viral DNA can get turned on, and the cell starts to produce new virus. This is why medication adherence is critical. Stopping medication, even for a short time, might result in new cells being infected with HIV. Researchers are working hard to find a true cure for HIV that could completely eradicate the virus from an infected person.
HIV The small green dot to the left of the T cell is a HIV particle, shown to scale. Antiretroviral therapy and the search for a cure. Some antiretroviral drugs block HIV from entering new cells.
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IDM is committed to utilizing modeling approaches and quantitative analysis to explore how interventions can act to reduce the burden and transmission of HIV. This page provides information about HIV itself: the biology, symptoms, treatment, and prevention.
The human immunodeficiency virus HIV attacks the immune system by targeting CD4 positive T cells, which are white blood cells that serve a crucial role in regulating immune response and fighting off infection.
When left untreated, HIV drastically reduces the number of CD4 cells, severely weakening the immune system and enabling opportunistic infections and cancers. There is no cure for HIV, but it is possible to treat and control the virus. Scanning electromicrograph of an HIV-infected T cell.
HIV is a retrovirus. The virus integrates viral DNA into the chromosomal DNA of the host cell, becoming a permanent part of the host genome. The cellular machinery of host cells is sequestered by the virus to replicate new viral particles.
HIV is a particular type of retrovirus called a lentivirus. Characterized by long incubation periods, these viruses cause chronic and deadly diseases in mammals; in primates, they target CD4 proteins of the immune system. Host cells are destroyed in the process of viral replication, causing a significant reduction in immune system cells as viral load increases. As these vital immune system cells are destroyed, cell-mediated immunity is lost and the individual becomes increasingly susceptible to opportunistic infections.
HIV is a spherical retrovirus with a typical diameter between and nm—about 60 times smaller than a red blood cell. A viral envelope, or lipid membrane, encloses the virion. Embedded in this lipid membrane are 72 envelope proteins, glycoproteins , which spike through the membrane. These surface proteins, gp and gp41 , are responsible for viral attachment and entry to host cells. Within the membrane is a capsid , which contains enzymes and genetic material.
The enzymes, required for virion replication, are reverse transcriptase , proteases , ribonuclease , and integrase. Three genes code for structural proteins required for creating new viral particles. Diagram illustrating the structure of the HIV genome. The replication process to create new HIV virions occurs in three phases. First, the virus needs to enter the host cell.
Second, replication of viral genetic information occurs within the host cell. And third, and finally, new virions are assembled and released from the host cell.
Ultimately, host cells are destroyed by HIV infection, but this destruction is not the result of the release of mature virions. Instead, infected cells appear to sacrifice themselves through a highly inflammatory form of apoptosis called pyroptosis [Ref1] , [Ref2].
In order to enter a host cell, the HIV virion uses the glycoproteins on its surface to attach to the target cell. Once fusion is complete, the capsid which contains the RNA, reverse transcriptase, proteases, ribonuclease, and integrase is injected into the host cell. This process is represented in steps one and two in the above figure.
This process is represented in steps three, four, and five in the above figure. It is worth noting that the process of reverse transcriptase is extremely error-prone. The mutations arising out of these copying errors are thought to contribute to the development of drug resistance and to also enable the virus to escape detection by the immune system.
Once the new copies of viral proteins and genomic RNA have been created, they move to the surface of the host cell. Viral structural proteins created from the Gag gene associate with the inner surface of the host cell, causing a new virion to start forming and bud from the cell.
As the bud progresses, viral proteases cleave the structural components so they can be assembled to form a the capsid and other capsid enzymes. This process is represented in steps six and seven in the above figure.
A hallmark of HIV is the high level of genetic variability the virus exhibits, which can make treatment very difficult. Both types follow the same transmission route and have the same pathology—both may develop into AIDS. Image credit: Thomas Splettstoesser www. It is thought that each of these groups corresponds to an independent transmission event of SIV simian immunodeficiency virus into humans [Ref4]. It can further be divided into 11 subtypes, A through K. Recombination between subtypes can also occur, further increasing genetic diversity of HIV.
Many of the subtypes have been identified due to differences in the envelope env region—the genes that code for gp and gp Disease progression is slower, and in some cases infected individuals may remain lifelong non-progressors. HIV-2 has 8 known subgroups: A through H.
HIV is difficult to treat, largely due to how genetically diverse it is, and how rapidly it can increase diversity. This arises due to multiple reasons:. Unfortunately, there are no distinctive symptoms used to diagnose HIV. The only definitive method of diagnosis is through testing. Some individuals may experience flu-like symptoms such as fever, chills, rash, night sweats, achy muscles, sore throat, fatigue, etc in the first weeks after infection, but not every infected individual experiences symptoms, and these symptoms are not conclusive.
For those experiencing symptoms, they may persist for a few days up to several weeks. In this early period, HIV tests may not yield a positive result even though the person is infectious.
Two to four weeks after infection, individuals may experience flu-like illness. During this period, the virus is still active but reproduction has slowed, and typically no symptoms are exhibited. Because the immune system is severely damaged, individuals succumb to increasing numbers of severe illnesses opportunistic infections. Without treatment, survival with AIDS is roughly 3 years. Many myths—and stigmas—persist around how HIV is transmitted. Understanding how it is—and is not—transmitted is key for the success of control efforts.
HIV has specific transmission routes and it only survives in particular bodily fluids: blood, semen, pre-seminal fluid, rectal and vaginal fluids, and breast milk. While certain behaviors can increase risk of HIV such as unprotected sex or sharing needles , other factors, such as co-infection with other STDs, can also increase the chances of HIV transmission.
This is because STDs can cause irritation of the skin, sores, etc, which makes it easier for HIV to enter the bloodstream. Even just irritation of the genital areas can increase the risk, as it increases the number of cells that can serve as targets for HIV. Additionally, there are treatments that will prevent transmission, which can be especially important for serodifferent partners. PrEP reaches its maximum protection effectiveness at about 7 days of daily use for receptive anal sex, and at about 20 days of daily use for receptive vaginal sex and injective drug use.
Currently, there little to determine how long it takes to reach maximum protection for insertive anal or insertive vaginal sex; current information can be found with the Risk Reduction Tool.
These combinations are comprised of nucleoside reverse transcriptase inhibitors NRTIs , nonnucleoside reverse transcriptase inhibitors NNRTIs , protease inhibitors , entry inhibitors , and integrase inhibitors. Using a multi-faceted approach with different drug combinations has helped prevent drug resistance in patients.
ART should also be taken to help prevent transmission from infectious to uninfected individuals. ART prevents transmission by reducing viral load to undetectable levels. However, caution should still be taken as HIV is theoretically still transmissible, despite having undetectable viral loads. HIV can still exist in semen, vaginal or rectal fluids, breast milk, or other parts of the body—viral load tests only measure viral load in blood see Testing.
Further, viral load may increase between tests, making transmission possible even after a test with an undetectable load. Finally, STDs increase viral load in genital fluids; so having an STD and HIV may increase risk of transmitting to partners even if viral load is undetectable in blood.
As of , there are an estimated 1. According to the WHO, globally there were over 1. Despite progress with these programs, there is still much room for improvement. Achievement of these goals will facilitate ending the worldwide AIDS epidemic by Testing is a key step in acheving these goals, as many people living with HIV are unaware of their status. To achieve viral suppression, individuals living with HIV need to have reliable access to treatment.
With the goals, these numbers are expected to increase rapidly. However, while universal test and treat remains an important component of combination HIV Prevention [Ref15] , [Ref16] , there is growing skepticism as to whether the goals, and universal test and treat in general, will be sufficient to end the epidemic [Ref17].
Testing is the only definitive method for diagnosing HIV infection, making it the important first step for care. According to the CDC, everyone between the ages of should be tested at least once during routine care. No test is able to detect HIV immediately after exposure, so testing regimes need to be conducted on appropriate time-scales.
Since the start of the epidemic, the WHO estimates that over 70 million people have been infected, and 35 million have died. However, despite these efforts and advances, there is still much work to be done for HIV control. As of the end of , there are upwards of 34 million adults—approximately 0. The number of people worldwide living with HIV in , broken down by global region.
Image credit: Avert. Because HIV cannot be cured, there have been immense efforts placed on prevention of new infections. As of , there are still around 2 million new cases in adults [Ref20] and , cases in children each year [Ref11]. Despite the high numbers of individuals living with HIV, prevention efforts have been successful, as overall disease incidence is down.
In addition to prevention of new infections, control of HIV has also focused on the care of individuals living with HIV, in order to reduce mortality. Approximately 1 million people still die each year from HIV-related illnesses [Ref18]. Much of the success in prevention and treatment of HIV stems from advances in medication, namely the antiretrovirals that are available. The progress is remarkable, but the effort continues to halt the spread of HIV.
Ending the AIDS epidemic is a formidable challenge that requires a multifaceted and multi- disciplinary approach. While HIV treatment and prevention efforts are crucial components, mathematical modeling also plays a vital role.