Thursday, July 18, 2024

What Cells Does Hiv Infect

Preventive Treatment After Exposure

How HIV infects us: Mucous membranes, dendritic cells, and lymph nodes | Khan Academy

People who have been exposed to HIV from a blood splash, needlestick, or sexual contact may reduce the chance of infection by taking antiretroviral drugs for 4 weeks. These drugs are more effective when they are started as soon as possible after the exposure. Taking two or more drugs is currently recommended.

Doctors and the person who was exposed typically decide together whether to use these preventive drugs. They base the decision on the estimated risk of infection and the possible side effects of the drugs. If they do not know whether the source is infected with HIV, they consider how likely the source is to be infected. However, even when the source of the exposure is known to be infected with HIV, the risk of infection after exposure varies, depending on the type of exposure. For example, risk from a blood splash is less than that from a needlestick.

Immediately after exposure to HIV infection, what is done depends on the type of exposure:

  • If skin is exposed, it is cleaned with soap and water.

  • Puncture wounds are cleaned with antiseptic.

  • If mucous membranes are exposed, they are flushed with large amounts of water.

What Are The Factors That Affect Disease Progression

The most important factor affecting HIV progression is the ability to achieve viral suppression. Taking antiretroviral therapy regularly helps many people slow the progression of HIV and reach viral suppression.

However, a variety of factors affect HIV progression, and some people progress through the phases of HIV more quickly than others.

Factors that affect HIV progression can include:

  • Ability to achieve viral suppression. Whether someone can take their antiretroviral medications and achieve viral suppression is the most important factor by far.
  • Age when symptoms start. Being older can result in faster progression of HIV.
  • Health before treatment. If a person had other diseases, such as tuberculosis, hepatitis C, or other sexually transmitted diseases , it can affect their overall health.
  • Timing of diagnosis. Another important factor is how soon a person was diagnosed after they contracted HIV. The longer between their diagnosis and treatment, the more time the disease has to progress unchecked.
  • Lifestyle. Practicing an unhealthy lifestyle, such as having a poor diet and experiencing severe stress, can cause HIV to progress more quickly.
  • Genetic history. Some people seem to progress more quickly through their disease given their genetic makeup.

Some factors can delay or slow the progression of HIV. These include:

Living a healthy lifestyle and seeing a healthcare provider regularly can make a big difference in a persons overall health.

Hiv Promotes Survival Of Infected Genital T Cells By Upregulating Birc5

Finally, we postulated that for effective dissemination, the infected cell needs to survive for long enough to travel the distance to infect other cells. BIRC5 was recently shown to promote survival of HIV-infected PBMCs . We found that HIV targeted cells in the FRT with high levels of BIRC5 for infection, and then further upregulated this protein . These results highlight that HIV-infected genital T cells, like infected cells from PBMCs , express high levels of BIRC5, but importantly suggest that this reflects a combination of HIV selecting cells for high levels of BIRC5 and upregulating this anti-apoptotic factor.

HIV exploits BIRC5 for cell survival upon infection of genital T cells.

Collectively, these studies of remodeling support a model whereby HIV infection of genital T cells generates a population of infected Tem that exhibit enhanced survival due to BIRC5 expression but compromised TCR signaling. Based on the expression patterns of homing receptors, these infected cells are expected to disseminate to the lymphoid follicles of lymph nodes .

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Cancers Common In People With Hiv Infection

Kaposi sarcoma Kaposi Sarcoma Kaposi sarcoma is a skin cancer that causes multiple flat pink, red, or purple patches or bumps on the skin. It is caused by human herpesvirus type 8 infection. One or a few spots may appear… read more , a cancer caused by a sexually transmitted herpesvirus, appears as painless, red to purple, raised patches on the skin. It occurs mainly in men who have sex with men.

Cancers of the immune system . Often, lymph nodes in the neck, under the arms, or in the groin enlarge rapidly and painlessly… read more ) may develop, sometimes first appearing in the brain. When the brain is affected, these cancers can cause weakness of an arm or a leg, headache, confusion, or personality changes.

Having AIDS increases the risk of other cancers. They include cancer of the cervix, anus, testes, and lungs as well as melanoma and other skin cancers. Men who have sex with men are prone to developing cancer of the rectum due to the same human papillomaviruses Human Papillomavirus Infection Human papillomavirus causes warts. Some types of HPV cause skin warts, and other types cause genital warts . Infection with some HPV… read more that cause cancer of the cervix in women.

How Does Acute Hiv Affect The Body

Hiv Infected Cell Photograph by Steve Gschmeissner/science ...

Once a person contracts HIV, the acute infection takes place immediately.

Symptoms of the acute infection may take place days to weeks after the virus has been contracted. During this time, the virus is multiplying rapidly in the body, unchecked.

This initial HIV stage can result in flu-like symptoms. Examples of these symptoms include:

However, not all people with HIV experience initial flu-like symptoms.

The flu symptoms are due to the increase of copies of HIV and widespread infection in the body. During this time, the amount of CD4 cells starts to fall very quickly. The immune system then kicks in, causing CD4 levels to rise once again. However, the CD4 levels may not return to their pre-HIV height.

In addition to potentially causing symptoms, the acute stage is when people with HIV have the greatest chance of transmitting the virus to others. This is because HIV levels are very high at this time. The acute stage typically lasts between several weeks and months.

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Preventive Treatment Before Exposure

Taking an antiretroviral drug before being exposed to HIV can reduce the risk of HIV infection. Such preventive treatment is called preexposure prophylaxis . However, PrEP is expensive and is effective only if people take the drug every day. Thus, PrEP is recommended only for people who have a very high risk of becoming infected, such as people who have a partner who is infected with HIV.

PrEP may also be recommended for people who engage in high-risk sexual activities, such as the following:

  • Men who have anal sex with men without using a condom

  • Heterosexual men and women who do not regularly use condoms during sex with partners whose HIV status is unknown and who are at increased risk of HIV infection

People who use PrEP still need to use other methods to prevent HIV infection, including consistent use of condoms and not sharing needles to inject drugs.

Diagnosis Of Hiv Infection

  • Tests to detect antibodies to the HIV virus in a sample of blood or saliva

  • Tests to detect HIV RNA in a sample of blood

Early diagnosis of HIV infection is important because it makes early treatment possible. Early treatment enables infected people to live longer, be healthier, and be less likely to transmit HIV to other people.

Doctors usually ask about risk factors for HIV infection Transmission of HIV Infection Human immunodeficiency virus infection is a viral infection that progressively destroys certain white blood cells and can cause acquired immunodeficiency syndrome . HIV is transmitted… read more and about symptoms .

Doctors also do a complete physical examination to check for signs of opportunistic infections, such as swollen lymph nodes and white patches inside the mouth , and for signs of Kaposi sarcoma of the skin or mouth.

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Strategies For Preventing The Transmission Of Hiv

  • Abstain from sexual activity.

  • Use a latex condom for each act of intercourse with an infected partner or a partner whose HIV status is unknown .

  • For men engaging in oral sex, withdraw before ejaculation.

  • For men, get circumcised .

  • For newly monogamous couples, get tested for HIV infection and other sexually transmitted diseases before engaging in unprotected sexual intercourse.

  • Never share needles or syringes.

  • Wear rubber gloves when touching body fluids of another person .

  • If accidentally exposed to fluids containing HIV , seek treatment with antiretroviral drugs to prevent infection.

Condoms made of latex provide good protection against HIV , but they are not foolproof. Oil-based lubricants should not be used because they may dissolve latex, reducing the condom’s effectiveness.

Other measures can help. For men, circumcision, an inexpensive, safe procedure, reduces the risk of becoming infected during vaginal intercourse with an infected woman by about half. Whether circumcision reduces the risk of HIV infection in other circumstances is unclear. Because circumcision provides only partial protection against HIV infection, people should also use other measures to prevent HIV infection. For example, if either partner has a sexually transmitted disease or HIV infection, it should be treated, and condoms should be used correctly and consistently.

Preventing Transmission By Blood Transfusions And Organ Transplants

How HIV Infects Cells: An Introduction

In the United States, the following have almost eliminated transmission of HIV infection by organ transplantation or blood transfusion:

  • Screening donors of organs or blood for risk factors for HIV infection

  • Screening donated blood for HIV

Risk is reduced further by asking people with risk factors for HIV infection, regardless of their test results for HIV, not to donate blood or organs for transplantation.

However, developing countries have not consistently used sensitive HIV screening tests and have not restricted donors. Consequently, transmission by these routes is still a problem in these countries.

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Respiratory And Cardiovascular Systems

HIV makes it hard to fight off respiratory problems such as the common cold and flu. In turn, an HIV-positive person may develop related infections, such as pneumonia.

Without treatment for HIV, advanced disease puts an HIV-positive person at an even greater risk for infectious complications, such as tuberculosis and a fungal infection called pneumocystis jiroveci pneumonia .

PJP causes trouble breathing, cough, and fever.

The risk of lung cancer also increases with HIV. This is due to weakened lungs from numerous respiratory issues related to a weakened immune system.

According to available research , lung cancer is more prevalent among people with HIV compared to people without it.

People with HIV are more likely to develop high blood pressure. HIV also raises the risk of pulmonary arterial hypertension . PAH is a type of high blood pressure in the arteries that supply blood to the lungs. Over time, PAH will strain the heart and can lead to heart failure.

If a person has HIV with a low CD4 count, theyre also more susceptible to tuberculosis .

TB is an airborne bacterium that affects the lungs. Its a leading cause of death in people who have AIDS. Symptoms include chest pain and a bad cough that may contain blood or phlegm. The cough can linger for months.

Hiv Remodels Genital T Cells To Impair Tcr Signaling And Promote Dissemination Of Infected Cells

Having described the phenotypes of HIV-susceptible ETs, we next assessed how HIV modulates expression of specific receptors on these cells during infection by comparing antigen expression in PRE versus infected cells . For example, an antigen that is expressed at higher levels on cells selected for infection would exhibit a higher median signal intensity on PRE cells than on uninfected cells . If infection does not modulate expression of that antigen, its MSI would be the same in the PRE and infected cells . If, however, the antigen is downregulated as a result of infection, then its MSI will be lower on infected cells relative to PRE cells . Figure 5Aiii shows an additional hypothetical example of an antigen whose expression levels are equivalent on the total population of uninfected cells and on cells preferentially infected by HIV, but are then downregulated as a result of infection.

HIV remodels cells to impair TCR signaling and promote migration of infected cells to lymph node follicles.

We went on to study whether any modulations that might promote systemic spread of the virus could be identified. The integrin 41 directs CD4+ T cells to the FRT . Although we did not see differences in 1 expression between uninfected, PRE, or infected cells, there was selection of 4low cells for infection, followed by further down-regulation of 4 after infection . These events may facilitate exit of the infected cells from the genital tract.

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The Human Immunodeficiency Viruses

The HIVs are members of the lentivirus subgroup of the Retroviridae family. They are RNA viruses that posses the enzyme reverse transcriptase . This enzyme allows the virus to reverse-transcribe its own RNA, and the resultant complementary DNA is incorporated into the cellular DNA of the host. Two main types of HIV exist: HIV-1 and HIV-2, which differ in genomic structure and antigenicity as well as in their latent period as pathogenicity. HIV-1 was identified, as the causative agent of AIDS, by three different groups in the early eighties. These were Montagniers at the Pasteur Institute in Paris , Gallos at the National Institute of Health USA, and Levys at the University of California San Francisco , USA. The HIVs were initially called LAV , HTLV-III-human T lymphotropic virus and ARV .,, In 1986 a second virus was identified, and the original was renamed HIV-1 to distinguish them. The diameter of the HIV virion is approximately 100 nm and electron microscopy studies have revealed a characteristic cylindrical core in HIV particles surrounded by an outer envelope .

Electron micrograph of HIV-1 and HIV-2 .

HIV-1 virions are shown budding . HIV-2 virions are shown in . Magnification is 100,000 x. Scale bar =100nm.

This electron microscopy was kindly performed by Dr. Robert Dourmashkin.

Eradication Strategies Targeting The Transcriptionally Latent Reservoir

HIV infected T

Even though ART has significantly increased life expectancy of HIV-1 infected individuals, complete eradication of the virus is not achievable without targeting the HIV-1 latent reservoirs. Currently, several therapeutic strategies are explored and early findings suggest that different strategies may be required to eliminate the different cellular viral reservoirs: memory CD4+ T cells which importantly maintain the viral reservoir through homeostatic- or antigen specific proliferation, and long lived cells like macrophages residing in the tissue.

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Simplified Life Cycle Of The Human Immunodeficiency Virus

Like all viruses, human immunodeficiency virus reproduces using the genetic machinery of the cell it infects, usually a CD4+ lymphocyte.

  • HIV first attaches to and penetrates its target cell.

  • HIV releases RNA, the genetic code of the virus, into the cell. For the virus to replicate, its RNA must be converted to DNA. The RNA is converted by an enzyme called reverse transcriptase . HIV mutates easily at this point because reverse transcriptase is prone to errors during the conversion of viral RNA to DNA.

  • The viral DNA enters the cells nucleus.

  • With the help of an enzyme called integrase , the viral DNA becomes integrated with the cells DNA.

  • The DNA of the infected cell now produces viral RNA as well as proteins that are needed to assemble a new HIV.

  • A new virus is assembled from RNA and short pieces of protein.

  • The virus pushes through the membrane of the cell, wrapping itself in a fragment of the cell membrane and pinching off from the infected cell.

  • To be able to infect other cells, the budded virus must mature. It becomes mature when another HIV enzyme cuts structural proteins in the virus, causing them to rearrange.

Drugs used to treat HIV infection were developed based on the life cycle of HIV. These drugs inhibit the three enzymes that the virus uses to replicate or to attach to and enter cells.

HIV also infects other cells, such as cells in the skin, brain, genital tract, heart, and kidneys, causing disease in those organs.

Resistance To Hiv Infection

The poorly understood phenomenon associated with the HIV-1 epidemic is the existence of individuals who have been repeatedly exposed to the virus but remain uninfected. It has been suggested that HIV-1 resistant individuals may have a non functioning co-receptor preventing the virus from entering cells., The CCR-5 receptor was demonstrated as one of the main co-receptors for NSI strains of HIV-1. Samson et al., reported that a 32 bp deletion within the coding region for the CCR-5 generating a non-functional receptor that did not support infection by NSI strains of HIV-1. Moreover, white blood cells from individuals homozygous for the mutant CCR-5 were found to be highly resistant to infection by NSI viruses., Population studies indicate that the homozygous defect is found in only 1% of Caucasians of western European ancestry whereas the heterozygous defect is present in approximately 20% of this population. These results indicate that variants of the CCR-5 receptor could be responsible for the relative resistance to HIV-1 infection exhibited by some individuals and also for the variability of the course of the disease in infected patients.

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V3 Loop Of The Glycoprotein 120

Before HIV is able to gain entry into a target susceptible cell, the third hypervariable region loop of the surface glycoprotein gp120 molecule has been implicated as an important factor for cell tropism and for cell fusion. The determinants of HIV tropism can be mapped to the viral envelope gene, thus indicating that tropism is restricted at the level of virus entry. A significant finding was that a major determinant of HIV-1 tropism is the V3 region of the surface gp120. The HIV-1 envelope gene is approximately 2.5 Kb in length and gp120 has a 1.6 Kb nucleotide sequence. The gp120 is divided into six constant and five hyper-variable regions ., Studies have already shown that mutations in the V3 loop are essential in cellular tropism and in the antigenicity of gp120. The V3 loop, known as the principal neutralising domain , is considered to be the major immunodominant region of the gp120 for both HIV-1, and HIV-2. This domain induces neutralising antibodies and is the target for cytotoxic T lymphocyte killing. Neutralising antibodies are able to block infection in vitro by blocking fusion of the virus. The acquisition of the syncytium inducing phenotype is linked to substitutions of acidic or neutral amino acids by more basic amino acids in the V3 loop.

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