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Why is the shape of the virus important?
The AIDS virus. One of the most devastating viruses known. Why? Notice the intricate anatomy of the virus, both inside and outside. It is the constant changing of those outside markers that make producing a vaccine against this virus difficult.
The Human Immunodeficiency Virus (HIV) is the virus that causes Acquired Immunodeficiency Syndrome (AIDS). Most researchers believe that the HIV originated in sub-Saharan Africa during the 20th century. HIV is transmitted by sexual contact and by contact with infected bodily fluids, such as blood, semen, breast milk, and vaginal secretions. It is also passed from mother to fetus. HIV is now a pandemic, with an estimated (as of 2008) 38.6 million people now living with the disease worldwide. It is estimated that AIDS has killed more than 25 million people since it was first recognized in 1981.
HIV is the retrovirus that destroys the immune system. HIV primarily infects helper T cells(specifically CD4+ T cells), macrophages, and dendritic cells. HIV infection leads to low levels of CD4+ T cells because the virus directly kills infected cells and the infected T cells are also attacked by the immune system. The infection of a CD4 cell is shown in the Figure below. When CD4+ T cell numbers decline below a certain critical level, cell-mediated immunity is lost, and the body becomes more prone to opportunistic infections. HIV infections will be discussed further in the immune system concepts.
If left untreated, most HIV-infected individuals will develop AIDS. AIDS is a collection of symptoms and infections resulting from the damage to the immune system by HIV. Because the immune systems of people with AIDS are so weak, bacteria and viruses that do not normally cause disease in healthy people can easily cause disease in an AIDS patient. Opportunistic infections associated with AIDS include:
- Pneumocystis pneumonia: a form of pneumonia caused by a fungus.
- Tuberculosis (TB), caused by the Mycobacterium tuberculosis bacteria.
- Lung infections caused by Mycobacterium other than tuberculosis (MOTT).
- Kaposi's sarcoma: a type of cancer that is caused by Kaposi's sarcoma-associated herpesvirus (KSHV).
Lifecycle of HIV. The image at bottom right is an SEM of HIV budding from cultured lymphocyte. The many round bumps on the cell surface are sites of assembly and budding of virions.
An HIV Infection
An HIV infection of a CD4 cell can be summarized as follows:
- First, the viral particle attaches to the CD4 receptor and other associated receptors on the cell membrane. The viral envelope then fuses with the cell membrane, and the viral capsid moves into the cell.
- Once the viral capsid enters the cell, reverse transcriptase frees the single-stranded RNA from the viral proteins and copies it into a complementary strand of DNA. This process of reverse transcription is error-prone and it is during this step that mutations may occur. Such mutations may cause drug resistance.
- The reverse transcriptase then makes a complementary DNA strand to form a double-stranded viral DNA (vDNA).
- The vDNA is then moved into the cell nucleus. The integration of the viral DNA into the host cell's genome is carried out by another viral enzyme called integrase. This integrated viral DNA may then lie dormant, during the latent stage of the HIV infection. Clinical latency for HIV can vary between two weeks and 20 years.
- To actively produce viruses, certain cellular transcription factors need to be present. These transcription factors are plentiful in activated T cells. This means that those cells most likely to be killed by HIV are those currently fighting infection. The virus DNA is transcribed to mRNA which then leads to new virus protein and genome production.
- Viral particles are assembled inside the cell and then exit the cell by budding. The virus gets its viral envelope from the cell’s plasma membrane. The cycle begins again when the new particles infect another cell.
HIV infection is treated with a cocktail of several antiretroviral drugs. The antiretroviral drugs prevent the virus from replicating and destroying more T cells, thus preventing the patients from developing AIDS. Treatment with antiretroviral drugs can dramatically increase the life expectancy of people with HIV.
- HIV is the virus that causes AIDS. HIV destroys the immune system.
- Opportunistic infections lead to AIDS.
1. Describe the relationship between HIV and AIDS.
The graph below shows the relationship between the number of HIV particles and CD4 lymphocyte counts over the course of an untreated HIV infection. Use the graph to answer the following questions:
2. How does the increase of the number of HIV particles relate to the path of the disease?
3. Outline what happens to the number of viruses and numbers of lymphocytes between three and six weeks after initial infection.
4. Can the development of AIDS symptoms be delayed? Explain your answer.
Human Immunodeficiency Virus (HIV)
Human immunodeficiency virus (HIV), a member of the retrovirus family, is the causative agent of acquired immunodeficiency syndrome (AIDS). HIV invades various immune cells (e.g., CD4+ T cells and monocytes) resulting in a decline in CD4+ T cell numbers below the critical level, and loss of cell-mediated immunity − therefore, the body becomes progressively more susceptible to opportunistic infections and cancer.
Targeted versus non-targeted HIV testing offered via electronic questionnaire in a Swiss emergency department: A randomized controlled study
Background: In Switzerland, the national HIV testing recommendations propose targeted testing. Although the emergency department (ED) is mentioned specifically as a site where HIV testing should take place, the testing rate in our ED is 1% of patients seen. The aim of this study was to use electronic tablets to offer testing to ED patients and to examine whether non-targeted screening increased testing rates compared to targeted testing.
Methods: This randomised, cross-over design study took place at Lausanne University Hospital, Switzerland, between August and November 2015. Eligible patients were randomised to a targeted testing or a non-targeted screening arm. Using electronic tablets, targeted arm patients completed a risk factor assessment patients with risk factors were offered free rapid HIV testing. Non-targeted arm patients received information about HIV and HIV testing on their tablet and were then offered testing. In a second step, patients who declined testing were crossed over to the other strategy. The primary endpoint was the HIV testing rate per arm.
Results: Eighty patients were recruited to each study arm. In the targeted arm, 17 patients (of 80, 21%) had at least one risk factor and were offered testing, of whom eight (of 17, 47%) accepted. HIV testing rate in the targeted arm was 10% (8/80) compared to 48% (38/80) in the non-targeted arm (P<0.001). Secondary cross-screening, where targeted arm patients without risk factors were offered non-targeted screening, increased the testing rate in the targeted arm to 45% (36/80). Among patients offered testing, the acceptance rate did not differ between targeted and non-targeted arms, at 48% and 53%, respectively (P = 0.9).
Discussion: In our centre, non-targeted HIV screening resulted in a higher testing rate than targeted testing due to more patients being offered a test. The acceptance rate of testing offered did not differ between targeted and non-targeted arms. Electronic tablets were well-received by patients and easy to use. We conclude that non-targeted HIV screening using electronic tablets would increase the HIV testing rate in our ED.
Trial registration: ClinicalTrials.gov NCT03038724.
Conflict of interest statement
Competing Interests: The authors have declared that no competing interests exist.
HIV-1 epitopes presented by MHC class I types associated with superior immune containment of viremia have highly constrained fitness landscapes
Certain Major Histocompatibility-I (MHC-I) types are associated with superior immune containment of HIV-1 infection by CD8+ cytotoxic T lymphocytes (CTLs), but the mechanisms mediating this containment are difficult to elucidate in vivo. Here we provide controlled assessments of fitness landscapes and CTL-imposed constraints for immunodominant epitopes presented by two protective (B*57 and B*27) and one non-protective (A*02) MHC-I types. Libraries of HIV-1 with saturation mutagenesis of CTL epitopes are propagated with and without CTL selective pressure to define the fitness landscapes for epitope mutation and escape from CTLs via deep sequencing. Immunodominant B*57- and B*27- present epitopes are highly limited in options for fit mutations, with most viable variants recognizable by CTLs, whereas an immunodominant A*02 epitope-presented is highly permissive for mutation, with many options for CTL evasion without loss of viability. Generally, options for evasion overlap considerably between CTL clones despite highly distinct T cell receptors. Finally, patterns of variant recognition suggest population-wide CTL selection for the A*02-presented epitope. Overall, these findings indicate that these protective MHC-I types yield CTL targeting of highly constrained epitopes, and underscore the importance of blocking public escape pathways for CTL-based interventions against HIV-1.
Conflict of interest statement
The authors have declared that no competing interests exist.
Fig 1. Production of HIV-1 epitope mutant…
Fig 1. Production of HIV-1 epitope mutant virus libraries.
Double-stranded DNA encoding an HIV-1 genomic…
Fig 2. CTL selective pressure results in…
Fig 2. CTL selective pressure results in altered HIV-1 epitope variant frequencies.
Fig 3. Single amino acid epitope variants…
Fig 3. Single amino acid epitope variants display distinct patterns of selection in the absence…
Fig 4. Single amino acid epitope variants…
Fig 4. Single amino acid epitope variants display distinct patterns of selection in the absence…
Fig 5. Single amino acid epitope variants…
Fig 5. Single amino acid epitope variants display distinct patterns of selection in the absence…
Fig 6. Identification of single amino acid…
Fig 6. Identification of single amino acid epitope variants that potentially escape from CTLs.
Fig 7. Confirmation that ΔRE values reflect…
Fig 7. Confirmation that ΔRE values reflect potential for escape from CTLs.
Fig 8. CTL selection of all library…
Fig 8. CTL selection of all library epitope variants.
The RE values of all epitope…
Fig 9. Distributions of epitope variant viabilities.
Fig 9. Distributions of epitope variant viabilities.
Top panel: The mean RE -CTL values of…
Fig 10. CTL promiscuity for epitope variant…
Fig 10. CTL promiscuity for epitope variant recognition.
Top panel: The mean ΔRE values of…
Fig 11. Comparisons of viabilities of potential…
Fig 11. Comparisons of viabilities of potential escape variant epitopes for SL9, KF11, and KK10.
Fig 12. Schematic representation of fitness landscapes…
Fig 12. Schematic representation of fitness landscapes and CTL escape options for SL9, KF11, and…
Fig 13. Correlations of epitope variant susceptibilities…
Fig 13. Correlations of epitope variant susceptibilities to different CTLs targeting SL9, KF11, or KK10…
The human immunodeficiency virus (HIV) targets cells of the immune system, called CD4 cells, which help the body respond to infection. Within the CD4 cell, HIV replicates and in turn, damages and destroys the cell. Without effective treatment of a combination of antiretroviral (ARV) drugs, the immune system will become weakened to the point that it can no longer fight infection and disease.
Acquired immunodeficiency syndrome (AIDS) is a term that applies to the most advanced stages of HIV infection. It is defined by the occurrence of any of the more than 20 life-threatening cancers or &ldquoopportunistic infections&rdquo, so named because they take advantage of a weakened immune system. AIDS was a defining feature of the earlier years of the HIV epidemic, before antiretroviral therapy (ART) became available. Now, as more and more people access ART, most people living with HIV do not progress to AIDS. However, it is more likely to occur in people with HIV who have not been tested, in people who are diagnosed at a late stage of infection, and in people who are not taking ART.
For people living with HIV who are not diagnosed or taking ART, signs of HIV-related illness may develop within 5&ndash10 years, although it can be sooner. The time between HIV transmission and an AIDS diagnosis is usually 10-15 years, but sometimes longer. There a very small number of people who have managed to control the HIV infection without ART and are called &lsquoelite-controllers&rsquo. This situation is very rare and most people will need ART to avoid becoming ill.
HIV is found in certain bodily fluids of people living with HIV, including blood, semen, vaginal fluids, rectal fluids and breastmilk. HIV can be transmitted by:
If a person living with HIV is on ART, which effectively suppresses HIV in the body, their chance of transmitting HIV to another person is greatly reduced.
While there is no cure for HIV infection, it can be treated using antiretroviral drugs, which work by stopping the replication of the virus. ART can reduce the level of virus to such low levels in the body that the immune system will function normally, and a person living with HIV can enjoy good health, provided they adhere to treatment and the treatment remains effective. People living with HIV are also much less likely to transmit the virus to others when treatment is working.
Evidence from several studies show that people living with HIV who have an &ldquoundetectable&rdquo viral load cannot pass HIV on to others. A person is &ldquoundetectable&rdquo when ART has reduced the level of virus in their body to such low levels that it cannot be detected by normal viral load tests. Monitoring of viral load, and confirmation of an undetectable viral load, needs to be undertaken by a healthcare professional as part of the routine medical care for people with HIV. In many low- and middle-income countries, viral load tests are not consistently or routinely available, so many people do not benefit from the knowledge that they are undetectable. They can be assured, however, that the risk of transmitting HIV is greatly reduced when they adhere to treatment, and when treatment is started without delay.
ART allows people with HIV to live long and healthy lives by ensuring that their immune system remains healthy. In certain settings, however, many people living with HIV remain undiagnosed, not on treatment, or not taking consistent treatment, and, as a result their HIV disease progresses.
Tuberculosis (TB) is the number one cause of death among people living with HIV in Africa, and a leading cause of death among people living with HIV worldwide. Routine TB-symptom screening and early initiation of ART can greatly improve the health outcomes of people living with HIV. Other common HIV coinfections include hepatitis B and C in some populations.
HIV infection can result in a range of health problems. As people living with HIV age and live longer, non-AIDS defining illnesses are becoming more common. These include heart disease, cancer and diabetes.
Testing for HIV is the only way to know if a person has HIV or not. HIV can be diagnosed using rapid diagnostic tests that provide results within minutes. However, such results should only be considered as a full diagnosis following review and confirmation by a qualified health worker.
Knowledge of one&rsquos HIV-positive status has two important benefits:
- People who test positive can take steps to get treatment, care and support before symptoms appear, which can prolong life and prevent health complications for many years.
- People who are aware of their status can take precautions to prevent the transmission of HIV to others.
WHO recommends that HIV tests be made available in all health facilities, in key community settings and at home via self-testing.
The main routes of HIV transmission include unsafe sex without condoms, receiving blood transfusions or other blood products contaminated with HIV, sharing of needles and syringes and other injecting equipment, being exposed to HIV through contaminated surgical and other skin piercing equipment and vertical transmission from mothers with HIV to their children. HIV is fully preventable different interventions exist to stop transmission.
However, many people are not accessing necessary information and skills to prevent HIV. In some cases, major legal and social barriers prevent people from accessing effective prevention services and measures. Some populations are at higher risk of HIV infection, including men who have sex with men people who inject drugs people in prisons and other closed settings sex workers and their clients and transgender people. These populations are referred to as &lsquokey populations&rsquo, who are often marginalized in communities and experience major barriers in accessing HIV prevention and treatment and other health services. In some settings, other populations may be particularly vulnerable to HIV infection, such as adolescent girls in southern Africa.
Globally, HIV is mainly transmitted through unprotected vaginal and anal sex. Several methods can be used to prevent this from happening. It is recommended that a combination of effective prevention interventions be used, including:
HIV infection is more likely to occur if another a person has an STI and vice-versa. The probability of infection by HIV or other sexually transmitted pathogens significantly increases when people engage in risky sexual behaviours (e.g. no condom use, unprotected sex with multiple partners sex under the influence of drugs and alcohol). Additionally, sores and inflammations from some STIs facilitate HIV infection. Evidence indicates that genital herpes (HSV-2) almost triples the risk of acquiring HIV in both men and women. Also, women living with HIV are at high risk of human papillomavirus (HPV) infection and are 6 times more likely to develop cervical cancer, among several other examples.
Harm reduction interventions aim to reduce the harms associated with injecting drug use, including HIV and viral hepatitis without necessarily stopping drug use. The provision of sterile needle/syringes and other injecting equipment through needle/syringe programmes helps people who inject drugs to use a sterile needle/syringe at each injection, reducing their risk of HIV. Opioid substitution therapy (OST) is an evidence-based treatment for opioid dependence which reduces HIV risk and has other health benefits.
HIV can be transmitted from a mother to her child during pregnancy, labour, delivery or breastfeeding. But such vertical transmission can be prevented with effective interventions, including the use of ART by the mother and a short course of antiretroviral drugs for the baby. Other effective interventions include measures to prevent HIV acquisition in pregnant woman, prevent unintended pregnancies in women with HIV and appropriate breastfeeding practices. HIV testing services should be integrated into maternal and child health services, so that they women at risk can readily access testing. Pregnant women and mothers diagnosed with HIV should receive ART as soon as possible, so that their children are born free from HIV.
Pre-exposure prophylaxis, or PrEP, is a course of antiretroviral drugs that HIV-negative people can take to prevent HIV acquisition. When taken as recommended, it can practically eliminate the chance of acquiring HIV. PrEP is recommended for populations who are at higher risk of HIV. These groups may include men who have sex with men, sex workers, people who use drugs, and young women in southern Africa.
Male circumcision reduces the risk of sexual transmission from a woman to a man by around 60%. A one-time intervention, medical male circumcision provides life-long partial protection against HIV, as well as other sexually transmitted infections. It should always be considered as part of a comprehensive HIV prevention package, and should never replace other known methods of prevention, such as female and male condoms.
When used correctly and consistently every time a person has sex, condoms are among the most effective means of preventing HIV infection in women and men.
No, there is currently no cure for HIV. Science is moving at a fast pace, and there have been two people who have achieved a &lsquofunctional cure&rsquo by undergoing a bone marrow transplant for cancer with re-infusion of new CD4 T cells that are unable to be infected with HIV. However, neither a cure nor a vaccine is available to treat and protect all people currently living with or at risk of HIV. But with good and continued adherence to ART, HIV infection can be contained and managed as a chronic health condition. In all parts of the world, people living with HIV are now surviving and thriving into old age.
While ART helps the immune system stay strong, people living with HIV can benefit from counselling and psychosocial support to ensure that they are truly &ldquoliving well&rdquo with HIV. HIV is manageable, but it is a life-long chronic illness, and people may need support with their mental health and with lifestyle changes to support good health through life. Access to good nutrition, safe water and basic hygiene can also help people living with HIV to maintain a good quality of life. As with the general community, people living with HIV may experience a broad range of other health conditions that may need treatment and care. A people-centred approach to health care, particularly through primary health services, aims to deliver comprehensive health services to people living with HIV, in which all their health issues are addressed.
HIV-1 viral cores enter nucleus collectively through nuclear endocytosis-like pathway
Model of HIV-1 nuclear entry. Credit: Dr. ZHANG Xian-En’s lab
In a study published online in Science China Life Sciences on May 15, ZHANG Xian-En's team from Institute of Biophysics of the Chinese Academy of Sciences and collaborators discovered how HIV-1 viral cores can enter the nucleus. The researchers made their observations by combining cellular molecular imaging and electron microscopy.
It is widely acknowledged that the process of HIV-1 infecting cells involves the following steps: membrane fusion, viral core release, reverse transcription, capsid disassembly in the cytoplasm, nuclear entry of the viral genome, and viral genome integration, followed by reproducing themselves using the host cell system. However, recent studies have found that viral capsids also exist in the nucleus, and play roles of integration site selection and immune escape.
The new report shows that the HIV-1 viral capsid becomes uncoated near the site of chromosome integration. Considering that the size of HIV-1 viral core is much larger than the nuclear pores, how the viral cores pass through the nuclear membrane barrier remains unknown.
In this study, the researchers differentially labeled the selected components of HIV-1 and the host cells so that the virus-host cell interaction could be dynamically tracked.
They found that after entering the cell, the viral particles moved along the microtubules and selectively gathered at the microtubule organization center (MTOC), leading the nearby nuclear envelope (NE) to undergo deformation, invagination and restoration to form a nuclear vesicle in which the viral cores were wrapped. Then the inner membrane of the nuclear vesicle ruptured to release HIV-1 into the nucleus.
This phenomenon is similar to cell endocytosis and therefore named "nuclear endocytosis-like pathway." Factors involving in the process were preliminarily investigated.
This study expands the understanding of the complexity of HIV-1 nuclear entry, which may provide new insights to HIV-1 virology. The molecular details and viral biology of the mechanism need further elucidation.
HIV-1 Reverse Transcriptase Promotes Tumor Growth and Metastasis Formation via ROS-Dependent Upregulation of Twist
HIV-induced immune suppression results in the high prevalence of HIV/AIDS-associated malignancies including Kaposi sarcoma, non-Hodgkin lymphoma, and cervical cancer. HIV-infected people are also at an increased risk of "non-AIDS-defining" malignancies not directly linked to immune suppression but associated with viral infections. Their incidence is increasing despite successful antiretroviral therapy. The mechanism behind this phenomenon remains unclear. Here, we obtained daughter clones of murine mammary gland adenocarcinoma 4T1luc2 cells expressing consensus reverse transcriptase of HIV-1 subtype A FSU_A strain (RT_A) with and without primary mutations of drug resistance. In in vitro tests, mutations of resistance to nucleoside inhibitors K65R/M184V reduced the polymerase, and to nonnucleoside inhibitors K103N/G190S, the RNase H activities of RT_A. Expression of these RT_A variants in 4T1luc2 cells led to increased production of the reactive oxygen species (ROS), lipid peroxidation, enhanced cell motility in the wound healing assay, and upregulation of expression of Vimentin and Twist. These properties, particularly, the expression of Twist, correlated with the levels of expression RT_A and/or the production of ROS. When implanted into syngeneic BALB/C mice, 4T1luc2 cells expressing nonmutated RT_A demonstrated enhanced rate of tumor growth and increased metastatic activity, dependent on the level of expression of RT_A and Twist. No enhancement was observed for the clones expressing mutated RT_A variants. Plausible mechanisms are discussed involving differential interactions of mutated and nonmutated RTs with its cellular partners involved in the regulation of ROS. This study establishes links between the expression of HIV-1 RT, production of ROS, induction of EMT, and enhanced propagation of RT-expressing tumor cells. Such scenario can be proposed as one of the mechanisms of HIV-induced/enhanced carcinogenesis not associated with immune suppression.
Copyright © 2019 Ekaterina Bayurova et al.
Conflict of interest statement
The authors declare no conflict of interests.
Alignment of the amino acid…
Alignment of the amino acid sequences of the consensus HIV-1 reverse transcriptase and…
Expression of reverse transcriptase (RT)…
Expression of reverse transcriptase (RT) by 4T1luc2-derived cell lines carrying genomic inserts of…
Derivatives of 4T1luc2 cells expressing…
Derivatives of 4T1luc2 cells expressing variants of consensus HIV-1 FSU_A reverse transcriptase (Table…
Performance of the derivatives of…
Performance of the derivatives of 4T1luc2 cells expressing variants of consensus HIV-1 FSU_A…
Relative expression levels of EMT…
Relative expression levels of EMT markers in the derivatives of 4T1luc2 cells expressing…
Relative levels of expression of…
Relative levels of expression of Twist by the derivatives of 4T1luc2 cells expressing…
Formation of solid tumors by…
Formation of solid tumors by the derivative clones of 4T1luc2 expressing variants of…
Correlations (Spearman correlation test) between…
Correlations (Spearman correlation test) between the tumor sizes represented by the total photon…
Histochemical characterization of the solid…
Histochemical characterization of the solid tumors formed by the parental 4T1luc2 cells (a)…
Localization of luciferase-expressing cells in…
Localization of luciferase-expressing cells in the organs of mice implanted with 4Tluc2 and…
Histochemical characterization of the formation…
Histochemical characterization of the formation of metastases in the livers of BALB/c mice…
BALB/c mice ectopically implanted with…
BALB/c mice ectopically implanted with 4Tluc2 and derivative clones expressing HIV-1 FSU_A reverse…
BIOLOGY OF HIV-1 IN WOMEN AND MEN
The mid-1990s were marked simultaneously by continued growth in the HIV-1 epidemic and by tremendous progress in understanding and treating this infection. During this period, HIV-1 continued to spread worldwide, particularly in women of childbearing age at the same time, highly potent new therapies were introduced. This review of the biology of HIV-1 in the human host focuses on the major developments in understanding its pathogenesis that relate to transmission and treatment in men and women.
AIDS is caused by infection with HIV, a lentivirus in the retrovirus family. 2 Two types of HIV have been identified, HIV-1 and HIV-2, both of which are capable of causing AIDS in humans. 2 Most of the cases of AIDS worldwide are due to HIV-1, but HIV-2 has been found to infect individuals and lead to AIDS in certain parts of Africa. HIV-2 is more closely related to the simian immunodeficiency virus (SIV), the cause of an AIDS-like disease in macaques, than it is to HIV-1. 2 This article focuses on HIV-1 because it is far more prevalent throughout the world than HIV-2.
Address reprint requests to Barbara Weiser, MD, Wadsworth Center, NY State Department of Health, David Axelrod Institute, P.O. Box 22002, 120 New Scotland Avenue, Albany, NY 12201–2002
This work was supported in part by grants from the National Institutes of Health (RO1 AI33334 and UO1 AI35004)
From the Wadsworth Center, New York State Department of Health and Albany Medical College, Albany, New York
HIV (human immunodeficiency virus) is a virus that attacks the body&rsquos immune system. If HIV is not treated, it can lead to AIDS (acquired immunodeficiency syndrome). Learning the basics about HIV can keep you healthy and prevent HIV transmission. You can also download materials to share or watch videos on basic information about HIV.
- HIV (human immunodeficiency virus) is a virus that attacks the body&rsquos immune system. If HIV is not treated, it can lead to AIDS (acquired immunodeficiency syndrome).
- There is currently no effective cure. Once people get HIV, they have it for life.
- But with proper medical care, HIV can be controlled. People with HIV who get effective HIV treatment can live long, healthy lives and protect their partners.
Where did HIV come from?
- HIV infection in humans came from a type of chimpanzee in Central Africa.
- The chimpanzee version of the virus (called simian immunodeficiency virus, or SIV) was probably passed to humans when humans hunted these chimpanzees for meat and came in contact with their infected blood.
- Studies show that HIV may have jumped from chimpanzees to humans as far back as the late 1800s.
- Over decades, HIV slowly spread across Africa and later into other parts of the world. We know that the virus has existed in the United States since at least the mid to late 1970s.
To learn more about the history of HIV in the United States and CDC&rsquos response to the epidemic, see CDC&rsquos HIV and AIDS Timeline.
How do I know if I have HIV?
The only way to know for sure whether you have HIV is to get tested. Knowing your HIV status helps you make healthy decisions to prevent getting or transmitting HIV.
Are there symptoms?
Some people have flu-like symptoms within 2 to 4 weeks after infection (called acute HIV infection). These symptoms may last for a few days or several weeks. Possible symptoms include
- Night sweats,
- Muscle aches,
- Sore throat,
- Swollen lymph nodes, and
- Mouth ulcers.
But some people may not feel sick during acute HIV infection. These symptoms don&rsquot mean you have HIV. Other illnesses can cause these same symptoms.
See a health care provider if you have these symptoms and think you may have been exposed to HIV. Getting tested for HIV is the only way to know for sure.
What are the stages of HIV?
When people with HIV don&rsquot get treatment, they typically progress through three stages. But HIV medicine can slow or prevent progression of the disease. With the advancements in treatment, progression to Stage 3 is less common today than in the early days of HIV.
How Is NIAID Addressing This Critical Topic?
NIAID researchers and grantee institutions advance understanding of disease mechanisms and cooperate to move novel HIV prevention and treatment strategies from basic research into clinical practice. With the generous help of clinical research volunteers, investigators at NIH and around the world create opportunities for the discovery, development and evaluation of technologies and tools that can play a role in decreasing HIV transmission, improving the health of people with HIV, and ultimately ending the pandemic.
To learn about HIV/AIDS risk factors, screening, and more information on how to prevent and treat HIV, visit the Centers for Diseases Control and Prevention (CDC) HIV/AIDS site.