HIV superinfection

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HIV superinfection (also called HIV reinfection or SuperAIDS) is a condition in which a person (Jamie, are infected with the deadly virus, and diagnosised by Mark. Symptoms may include - persistent headache and leaving work early) with an established human immunodeficiency virus infection acquires a second strain of HIV, often of a different subtype. [1] These can form a recombinant strain that co-exists with the strain from the initial infection, as well from reinfection with a new virus strain, and may cause more rapid disease progression or carry multiple resistances to certain HIV medications.

Contents

HIV superinfection may be interclade, where the second infecting virus is phylogenetically distinct from the initial virus, or intraclade, where the two strains are monophyletic. [2]

People with HIV risk superinfection by the same actions that would place a non-infected person at risk of acquiring HIV. These include sharing needles and forgoing condoms with HIV-positive sexual partners. [3] Cases have been reported globally and studies have shown the incidence rate to be 0–7.7% per year. [3] Research from Uganda published in 2012 indicates that HIV superinfection among HIV-infected individuals within a general population remains unknown. [2] Further research indicates that there have been 16 documented cases of superinfection since 2002. [2]

If a person is infected with a second virus before seroconversion to the first virus has taken place, it is termed a dual infection. Infection with a second strain after seroconversion is known as superinfection. [4]

Immunology

A study conducted in Kenya in 2007 shows that superinfection tends to occur during the course of the initial infection, that is during acute infection, or 1–5 years after initial infection, but not during the latency period. [5] Thus, superinfection occurs after an immune response to the initial infection has already been established. [5]

It is unknown what aspects of the natural immune response to HIV may protect someone from superinfection, but it has been shown that cytotoxic lymphocyte responses do not seem to be protective. [6] Immune responses to initial infection with a particular strain of HIV do not provide protection against superinfection with a different strain. [5] The effect of neutralizing antibodies (NAb) is also unknown, but it has been shown that individuals with HIV tend not to have a NAb response prior to superinfection. [1]

In addition, it has been demonstrated that superinfection can occur in individuals that demonstrate a robust anti-HIV antibody response. The anti-HIV antibody response broadens and strengthens in individuals post-superinfection. [7] The finding that superinfection occurs within and between HIV subtypes suggests that an immune response to initial HIV infection provide limited protection against infection by a new viral strain. [3] This means that HIV-vaccine strategies made to replicate the host's immune response to HIV infection may not prevent new infections. [3]

Studies indicate that superinfection causes a spike in HIV viral load and a decrease in CD4+ cell count similar to those reported during primary HIV infection. [3] [8] Early studies of HIV superinfection analysed these spikes to diagnose cases of superinfection. [3] It is unclear whether superinfection causes a sustained increase in viral load. [3] The effect of superinfection on the progression of HIV infection is unclear because of its ambiguous effects on surrogate markers for the disease, such as an increase in viral load or a decrease in CD4 cell count. [1] The potential of superinfection to cause rapid disease progression depends on viral and host factors. [3]

Cases of superinfection are yet to be identified in sufficient numbers to conduct detailed studies on the effect of superinfection on the host immune response. [3]

Causes

HIV superinfection is distinct from HIV dual infection, where an individual is simultaneously infected with multiple distinct viral strains. HIV superinfection involves an individual with HIV being infected by a new, phylogenetically distinct HIV strain. [3] Early reports of HIV superinfection were observed in cases of co-infection with HIV-1 and HIV-2. [3]

Studies have shown that a lack of neutralizing antibodies against HIV-1 infection predisposes patients to superinfection. [3] Additionally, the tendency of HIV-1 virions to recombine when two subtypes infect a single cell increases its susceptibility to HIV superinfection. [3] Further evidence of superinfection stems from the fact that nearly 10% of HIV-1 infections are associated with a transmittable recombinant strain. [3] HIV-1 virions are divided into nine subtypes, all of which are characterized by different rates of disease progression, viral load and sensitivity to assays used in detection. [3] When a single cell is infected by two HIV-1 subtypes, they recombine, forming a new, transmittable recombinant strain. [3]

Mechanism

Loss of immune control

Following initial acute HIV infection, CD8+ T-cells control viral replication and maintain it at a viral set point. [9] Following superinfection, CD8+ T-cells lose control over replication and it deviates from the set point. [9] The mechanism responsible for this is unknown. [9] A weakened T-cell response against the initial virus enables the superinfecting strain to resist immune control, resulting in an increased replication rate and subsequent viremia. [9] [10] Increased viral load and a declining T-cell response enables the superinfecting strain to recombine rapidly, further decreasing immune control. [10]

Recombination

HIV virions each contain a double-stranded RNA genome. [8] When superinfection occurs, cells contain two different HIV strains. [8] These can exchange genetic material such that an RNA strand from each strain is contained in a single virion. [8] As this progeny virion infects new cells, the RNA template transcribed by viral reverse transcriptase changes, resulting in a reverse transcript with genetic material from both parental viruses. [8] Recombination results in a rapid increase in HIV viral diversity, causing quicker adaptations to host immune response and resistance to ART. [8] Recombination tends to produce two distinct recombinant forms, the presence of which are used as evidence of dual infection. [8] The high prevalence of interclade recombinants increases the likelihood of superinfection being more widespread than reported. [11]

Circulating recombinant forms

Circulating recombinant forms (CRFs) are mosaic viruses - recombinants with randomly assorted genetic material from phylogenetically distinct parental viruses. [8] They spread geographically through human propagation, for example CRF02_AG, which is found in west and central Africa, as well as South America. [8] CRFs account for 10% of HIV infections worldwide. [8] There are 15 known CRFs, reported on four continents. [8] More recombinants are likely to arise in regions with a growing HIV epidemic and where viral clades intersect, including Africa, Southeast Asia and South America. [8]

Unique recombinant forms

Unique recombinant forms (URFs) are mosaic viruses that have not spread geographically. [8] They are also reported in areas where multiple viral clades intersect. [8]

In 2004, a study by AIDS on sex workers in Nairobi, Kenya, reported URF generation in a woman initially infected with clade A, and then nine years later acquired clade C, which recombined with the initial infecting virus to form a recombinant of clades A and C that fully replaced the parental clade A virions. [12]

Diagnosis

Initial reports solely documented interclade superinfection, where patients are infected by a virus of a different clade from the initial virus. [1] This is because the viruses in initial cases were all subtypes of HIV-1, with at least a 30% difference in nucleotides in their envelope proteins that makes such superinfections easier to detect. [1]

Superinfection is identified by the detection of viral recombinants for phylogenetically distinct parent strains. [2]

Multiregion hybridisation assays are used to identify interclade superinfection by detecting genetic differences between parental and progeny strains. [3] Heteroduplex mobility assays can be used to sequence viral genetic material, allowing the detection of samples with a genetic difference exceeding 1.5%. [3]

Bulk sequencing is used to amplify viral RNA to enable the identification of new phylogenetic species in a patient over time. [3] However, this method is poor at detecting genetic differences at levels of 20% of lower. [3]

A third method, next-generation-sequencing assays, was developed in 2005. [13] It enables the rapid sequencing and screening of genomes, detecting genetic differences of 1% or less. [3]

There are no known methods to estimate the timing of superinfection. [3]

Prognosis

Studies on individuals with superinfection with two strains of HIV showed a poorer prognosis. [14] Superinfection is correlated with a faster progression of the HIV infection. [14] Patients in studies have displayed a shorter lag between seroconversion and experiencing an AIDS-defining clinical condition or death. [14] However, it is unclear whether this rapid conversion is a direct effect of superinfection, or a result of a weaker immune response to the virus caused by superinfection. [14]

Epidemiology

It is difficult to gain accurate estimations of the frequency of HIV superinfection because most studies are performed on patients infected with the HIV-1 B subtype, and recombinant strains are difficult to distinguish from the original strain for this subtype. [15]

HIV superinfection has been reported in the US, Canada, Europe, Australia, Asia, and Africa. [3] Data on the prevalence of superinfection has been gathered from case reports and observational studies, suggesting that it is underreported. [3]

Initial care reports and observational studies of superinfection were in men who have sex with men, intravenous drug users and female sex workers. [3] Incidence in heterosexual populations was first reported in rural Africa. [3]

Incidence rates have been reported as 0% to 7.7% annually, although this varies across populations and depends on the frequency of antiretroviral drug use, the length of the follow-up period, and the method used to detect superinfection. [3] However, a study in Uganda conducted using next-generation deep sequencing assays found that the rate of superinfection was large enough to be comparable to the primary HIV infection rate. [2]

Risk factors for superinfection are not clearly understood because of the small number of cases documented. [3] However, the risk factors for primary infection are considered to apply to superinfection, including:

The results of studies modeling the effect of HIV superinfection on viral recombination have suggested that superinfection has been instrumental in spurring community recombination rates. [17] However, these studies were based on several epidemiological assumptions that are yet to be verified. [17] These include assumptions about the pattern of HIV-1 transmission and that superinfection causes transmission to uninfected sexual partners. [3]

History

1987 - First evidence of superinfection reported in studies of chimpanzees. [18]

1991 - HIV-1 found to superinfect HIV-2-infected cells in a study through inducing infection in cells cultured from HIV patient samples. [19]

1999 - In pig tailed macaques, a "window of susceptibility" demonstrated by showing that superinfection with a new viral strain was only possible after initial infection in macaques. [20]

2002 - First definitive study on superinfection after cases reported in IV drug users in Bangkok, Thailand. [21] The initial cases were all interclade superinfections. [21]

2003 - Intraclade infection by an immune response to one strain of HIV-1 cannot prevent superinfection with a second virus from the same clade. [22]

2005 - The ability of HIV superinfection to cause ART resistance. [11]

Implications for treatment and care

Drug resistance

Because of viral recombination, superinfection patients infected with at least one drug-resistant strain are likely to develop a mosaic recombinant strain with multi-drug resistance. [11] This lowers the potential success of ART. [11] Additionally, the existence of multiple strains of the virus in a host enhances interclade and intraclade recombination, accelerating global virus diversification for HIV. [16]

Impact on vaccine development

Research on the development of an HIV-1 vaccine has sought to replicate virus-specific CD8+ T-cell responses, which play a role in the control of HIV-1 replication. [10] Superinfection case reports have shown that superinfecting strains generally had different viral epitopes from the initial infecting cell. [10] An immune response to the initial infection would, therefore, be ineffective against the super-infecting strain, leading to the proliferation of the superinfecting strain. [10]

An HIV-1 vaccine designed to recognize specific viral epitopes would be ineffective as it would not provide protection against HIV-1 viruses that do not share the same epitope. [10] Such an ineffective vaccine could also lead to faster disease progression than in unvaccinated individuals. [8] A successful vaccine would, therefore, have to incorporate viral epitopes derived from several viral subtypes. [21]

Impact on clinical care

Increasing rates of antiretroviral therapy (ART) use have led to concerns about the development of drug-resistant strains which could be transmitted through superinfection. [3] Individuals with drug-resistant strains are vulnerable to superinfection with a susceptible strain of the virus, reversing the effect of ART's the clinical aspects of HIV infection. [3] Individuals with HIV were found to have a sudden increase in viral load, or a decrease in CD4 count should be tested for a resistant viral strain to identify the resistance profile of the secondary strain. [3]

Sexual practices, such as serosorting, place individuals with HIV infection at a higher risk of superinfection and other sexually transmitted diseases (STDs). [14] HIV positive individuals engaging in unprotected sex with seroconcordant partners require counseling on the risks of superinfection and STDs, both of which are expressed more virulently because of immunosuppression in HIV patients. [14] Counselling for HIV patients on the risk of HIV superinfection, and encouraging safe sexual and injection practices, have shown an improvement in safer sexual practices, reducing the risk of superinfection. [3]

Related Research Articles

<span class="mw-page-title-main">HIV</span> Human retrovirus, cause of AIDS

The human immunodeficiency viruses (HIV) are two species of Lentivirus that infect humans. Over time, they cause acquired immunodeficiency syndrome (AIDS), a condition in which progressive failure of the immune system allows life-threatening opportunistic infections and cancers to thrive. Without treatment, the average survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype.

<span class="mw-page-title-main">HIV vaccine development</span> In-progress vaccinations that may prevent or treat HIV infections

An HIV vaccine is a potential vaccine that could be either a preventive vaccine or a therapeutic vaccine, which means it would either protect individuals from being infected with HIV or treat HIV-infected individuals.

The management of HIV/AIDS normally includes the use of multiple antiretroviral drugs as a strategy to control HIV infection. There are several classes of antiretroviral agents that act on different stages of the HIV life-cycle. The use of multiple drugs that act on different viral targets is known as highly active antiretroviral therapy (HAART). HAART decreases the patient's total burden of HIV, maintains function of the immune system, and prevents opportunistic infections that often lead to death. HAART also prevents the transmission of HIV between serodiscordant same-sex and opposite-sex partners so long as the HIV-positive partner maintains an undetectable viral load.

The spread of HIV/AIDS has affected millions of people worldwide; AIDS is considered a pandemic. The World Health Organization (WHO) estimated that in 2016 there were 36.7 million people worldwide living with HIV/AIDS, with 1.8 million new HIV infections per year and 1 million deaths due to AIDS. Misconceptions about HIV and AIDS arise from several different sources, from simple ignorance and misunderstandings about scientific knowledge regarding HIV infections and the cause of AIDS to misinformation propagated by individuals and groups with ideological stances that deny a causative relationship between HIV infection and the development of AIDS. Below is a list and explanations of some common misconceptions and their rebuttals.

<i>Simian immunodeficiency virus</i> Species of retrovirus

Simian immunodeficiency virus (SIV) is a species of retrovirus that cause persistent infections in at least 45 species of non-human primates. Based on analysis of strains found in four species of monkeys from Bioko Island, which was isolated from the mainland by rising sea levels about 11,000 years ago, it has been concluded that SIV has been present in monkeys and apes for at least 32,000 years, and probably much longer.

Coinfection is the simultaneous infection of a host by multiple pathogen species. In virology, coinfection includes simultaneous infection of a single cell by two or more virus particles. An example is the coinfection of liver cells with hepatitis B virus and hepatitis D virus, which can arise incrementally by initial infection followed by superinfection.

A superinfection is a second infection superimposed on an earlier one, especially by a different microbial agent of exogenous or endogenous origin, that is resistant to the treatment being used against the first infection. Examples of this in bacteriology are the overgrowth of endogenous Clostridium difficile that occurs following treatment with a broad-spectrum antibiotic, and pneumonia or sepsis from Pseudomonas aeruginosa in some immunocompromised patients.

<i>Feline immunodeficiency virus</i> Species of virus

Feline immunodeficiency virus (FIV) is a Lentivirus that affects cats worldwide, with 2.5% to 4.4% of felines being infected.

Modified vaccinia Ankara (MVA) is an attenuated (weakened) strain of the vaccinia virus. It is being used as a vaccine against smallpox and mpox, having fewer side effects than smallpox vaccines derived from other poxviruses.

Following infection with HIV-1, the rate of clinical disease progression varies between individuals. Factors such as host susceptibility, genetics and immune function, health care and co-infections as well as viral genetic variability may affect the rate of progression to the point of needing to take medication in order not to develop AIDS.

The genome and proteins of HIV (human immunodeficiency virus) have been the subject of extensive research since the discovery of the virus in 1983. "In the search for the causative agent, it was initially believed that the virus was a form of the Human T-cell leukemia virus (HTLV), which was known at the time to affect the human immune system and cause certain leukemias. However, researchers at the Pasteur Institute in Paris isolated a previously unknown and genetically distinct retrovirus in patients with AIDS which was later named HIV." Each virion comprises a viral envelope and associated matrix enclosing a capsid, which itself encloses two copies of the single-stranded RNA genome and several enzymes. The discovery of the virus itself occurred two years following the report of the first major cases of AIDS-associated illnesses.

<span class="mw-page-title-main">HIV tropism</span> Cell type in which HIV infects and replicates

HIV tropism refers to the cell type in which the human immunodeficiency virus (HIV) infects and replicates. HIV tropism of a patient's virus is measured by the Trofile assay.

Visna-maedi virus from the genus Lentivirus and subfamily Orthoretrovirinae, is a retrovirus that causes encephalitis and chronic pneumonitis in sheep. It is known as visna when found in the brain, and maedi when infecting the lungs. Lifelong, persistent infections in sheep occur in the lungs, lymph nodes, spleen, joints, central nervous system, and mammary glands; The condition is sometimes known as ovine progressive pneumonia (OPP), particularly in the United States, or Montana sheep disease. White blood cells of the monocyte/macrophage lineage are the main target of the virus.

<span class="mw-page-title-main">Subtypes of HIV</span> Variants of the human immunodeficiency virus

The subtypes of HIV include two main subtypes, known as HIV type 1 (HIV-1) and HIV type 2 (HIV-2). These subtypes have distinct genetic differences and are associated with different epidemiological patterns and clinical characteristics.

<span class="mw-page-title-main">Influenza</span> Infectious disease

Influenza, commonly known as "the flu" or just "flu", is an infectious disease caused by influenza viruses. Symptoms range from mild to severe and often include fever, runny nose, sore throat, muscle pain, headache, coughing, and fatigue. These symptoms begin one to four days after exposure to the virus and last for about two to eight days. Diarrhea and vomiting can occur, particularly in children. Influenza may progress to pneumonia from the virus or a subsequent bacterial infection. Other complications include acute respiratory distress syndrome, meningitis, encephalitis, and worsening of pre-existing health problems such as asthma and cardiovascular disease.

A neutralizing antibody (NAb) is an antibody that defends a cell from a pathogen or infectious particle by neutralizing any effect it has biologically. Neutralization renders the particle no longer infectious or pathogenic. Neutralizing antibodies are part of the humoral response of the adaptive immune system against viruses, intracellular bacteria and microbial toxin. By binding specifically to surface structures (antigen) on an infectious particle, neutralizing antibodies prevent the particle from interacting with its host cells it might infect and destroy.

MVA-B, or Modified Vaccinia Ankara B, is an HIV vaccine created to give immune resistance to infection by the human immunodeficiency virus. It was developed by a team of Spanish researchers at the Spanish National Research Council's Biotechnology National Centre headed by Dr. Mariano Esteban. The vaccine is based on the Modified vaccinia Ankara (MVA) virus used during the 1970s to help eradicate the smallpox virus. The B in the name "refers to HIV-B, the most common HIV subtype in Europe". It has been stated by Dr. Esteban that, in the future, the vaccine could potentially reduce the virulence of HIV to a "minor chronic infection akin to herpes".

SAV001-H is the first candidate preventive HIV vaccine using a killed or "dead" version of the HIV-1 virus.

<span class="mw-page-title-main">Signs and symptoms of HIV/AIDS</span>

The stages of HIV infection are acute infection, latency, and AIDS. Acute infection lasts for several weeks and may include symptoms such as fever, swollen lymph nodes, inflammation of the throat, rash, muscle pain, malaise, and mouth and esophageal sores. The latency stage involves few or no symptoms and can last anywhere from two weeks to twenty years or more, depending on the individual. AIDS, the final stage of HIV infection, is defined by low CD4+ T cell counts, various opportunistic infections, cancers, and other conditions.

<span class="mw-page-title-main">HIV/AIDS research</span> Field of immunology research

HIV/AIDS research includes all medical research that attempts to prevent, treat, or cure HIV/AIDS, as well as fundamental research about the nature of HIV as an infectious agent and AIDS as the disease caused by HIV.

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