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In 1983, a research team at the Pasteur Institute led by Luc Montagnier described a new retrovirus isolated from T-Lymphocytes of a patient with AIDS. After sending samples to the National Institutes of Health and having confirmation by Robert Gallo's research team the discovery was official. After arguments between the two teams over what the virus should be named a final decision was made in 1986, Human Immunodeficiency Virus or simply HIV (1). A member of the family Retroviridae, HIV is a Lentivirus which infects humans (2). Through replication, the virus leads to the destruction of the host's immune system as key components such as CD4+ T-Lymphocytes, become infected and eventually die. As the viral infection continues, the host becomes susceptible to opportunistic infections and is now considered to have Acquired Immunodeficiency Syndrome or AIDS. These opportunistic infections are the cause of death, not HIV, as the host is no longer able to combat against them with their weakened immune system. There are two types of HIV, the more common and virulent HIV-1, and the slower acting HIV-2. While HIV-2 is generally isolated to Western Africa, HIV-1 is found worldwide and has many subgroups associated with it. (1, 2).
The exact origin of HIV is unknown though it is widely accepted that HIV came from Simian Immunodeficiency Virus (SIV). SIV infects various primate species in the same way that HIV infects humans however; the simian hosts do not develop an immunodeficiency as we do (2). If it is accepted that SIV led to HIV, scientists still have to answer how the virus crossed species to initially infect humans. Currently, there are several theories of the initial infection ranging from contaminated vaccines, infection through the blood of hunted animals, and government conspiracies. As colorful and imaginative as some of these theories are, few have scientific evidence to back them up (1, 2).
HIV is an enveloped RNA virus with a diameter of approximately .1 microns. The envelope surrounding the virion particle is made up of a lipid bi-layer taken from previous host cells during the replication and budding process. Fastened to the envelope are various host cell proteins as well as the viral protein complex Env. The Env complex is comprised of two separate proteins: gp120 and gp41. These proteins enable the virion to attach itself to host cell receptors and infiltrate the cellular membrane. Inside the envelope resides a bullet shaped capsid constructed out of thousands of copies of viral protein p24. Inside the capsid are two single strands of RNA, both of which carry the nine genes of the virus (3 structural and 6 regulatory). In addition to RNA, the capsid contains three enzymes which are essential for viral replication: Protease, Reverse-transcriptase, and Integrase (3). Fig. 1 depicts a diagram of HIV showing the envelope, capsid, and location of genetic material and viral enzymes (4).
The replication of an HIV virion can be broken down into seven general steps. They include Attachment/Entry, Reverse Transcription, Integration, Transcription, Translation, Assembly, and Release/Maturation. The process begins when an HIV virion comes in contact with a host cell presenting CD4 receptors on its membrane. At this point Gp120 connects with the CD4 receptor through the help of a co-receptor (CCR5 or CXCR4). Once connected gp41 has a conformational change allowing the fusion of the two membranes. When the membranes fuse, the capsid is released into the cytoplasm. Here it is unraveled, exposing the two RNA strands as well as the three viral enzymes. With the strands of RNA released into the cytoplasm, Reverse Transcriptase activates converting one into double-stranded DNA. At this point, Integrase carries the viral DNA into the host cell's nucleus and inserts it into the genome creating a Provirus. The host cell, now permanently infected with HIV, begins transcribing its DNA (as well as the virus's) into mRNA. The mRNA leaves the cell's nucleus, and utilizes host cell machinery to translate the nucleic acid into new viral proteins and enzymes. During Assembly, viral proteins, RNA, and enzymes accumulate together near the cell membrane. The capsid is formed around the genome and enzymes and the immature virion buds from the cell. Membrane proteins on the host cell cut the bud off and release the new virion. During Maturation, the final enzyme Protease begins to work. Its job is to cleave the viral peptide chains into smaller proteins allowing the viral particle to become infectious. This replication cycle is repeated multiple times by each host cell, until their eventual death (5). Figure 2 taken from the National Institute of Allergy and Infectious Diseases shows the steps of the replication cycle carried out by HIV (3).
There are three primary phases of HIV-1 infection: Primary Infection, Chronic asymptomatic, and AIDS (1). Within each of these phases infected individuals may show various symptoms or none at all. During the Primary Infection, an individual's viral load is high due to rapid replication and the lack of antibodies present in the body. At this stage one is highly infectious and unfortunately, rarely knows they are carrying the virus. Symptoms are typically disguised as the flu or other infections and may include fever, fatigue, headache, and enlarged lymphnodes (3). These symptoms typically come about 2-6 weeks after infection and can last 2-3weeks. After the primary symptoms have passed, individuals become asymptomatic. This phase can last anywhere between 5-15+ years depending on the person who is classified accordingly as a rapid, typical, slow, or long-term progressor. During this time, HIV continues to replicate inside the body and slowly depletes the CD4+ T cell count. As the count falls below 200 cells/µl of blood the final phase AIDS occurs. It is in this last stage of the infection where opportunistic infections do their worse damage. The immune system is unable to fight off the pathogens and the risk of death is high (1, 3).
Testing & Diagnosis:
Because HIV has no unique symptoms to easily characterize it by, the only true way to know if you have been infected or not is to be tested. According the CDC and individual should be tested if they meet any of the following criteria
" Have you injected drugs or steroids or shared equipment (such as needles, syringes, works) with others?
Have you had unprotected vaginal, anal or oral sex with men who have sex with men, multiple partners, or anonymous partners?
Have you exchanged sex for drugs or money?
Have you been diagnosed with or treated for hepatitis, tuberculosis (TB), or a sexually transmitted disease (STD), like syphilis?
Have you had unprotected sex with someone who could answer yes to any of the above questions?
If you have had sex with someone whose history of sex partners and/or drug use is unknown to you or if you or your partner has had many sex partners, then you have more of a chance of being infected with HIV."(6)
Unfortunately, being tested does take planning. Though there is a Viral RNA Test which can be administered a few days after possible infection, it is expensive and only used in a few parts of the United States. The most common tests screen your body for antibodies which are developed in response to the viral antigens. It has been shown that antibody production for HIV can take anywhere from two weeks, to three months with some outliers as long as six months post-infection. With such a wide "window period" it can be difficult to determine if you are truly negative or secretly carrying HIV. Because of this, it is recommended an individual gets tested three months after the last possible exposure and once again at the 6 months mark. Besides the waiting period, the testing procedure is quick and can be painless. Using either a Rapid Oral Swab or traditional blood sample, results can arrive anywhere from twenty minutes to a few days. No matter which route is taken, if a result comes back positive and secondary test must be taken as confirmation (6).
Though there are no true vaccines or cures for HIV, treatments are available for those who become infected with the virus. Currently, there are approximately thirty-one FDA approved Anti-Retroviral Drugs (ARV's) for the treatment of HIV (3). These drugs are sub-divided into various classes depending on how they inhibit the virus. The Five Classes are: Reverse-Transcriptase Inhibitors, Protease Inhibitors, Fusion Inhibitors, Integrase Inhibitors, and lastly CCR5-Blocking Inhibitors (1). It is highly recommended that patients combine at least two separate classes of medications to effectively fight the progressive nature of HIV. Deemed HAART (Highly Active Antiretroviral Therapy) this treatment strategy counters HIV's ability to mutate and become resistant to a specific drug (3).
Students should be able to illustrate in detail the structure of a HIV virion. All major proteins, structures, and enzymes should be labeled accordingly.
Students should be able to explain the replication cycle of the HIV. This should include target cells, the processes of attachment and replication, and transmission from one host to another.
Fig. 1: Structure of HIV (4)
Fig. 2 Replication Cycle of HIV (3)