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Introduction
HIV and AIDS infection is one of those diseases that scare people because of the fact that it does not have cure. But when someone thinks that he or she has been infected, starting anti HIV medication may stop the infection completely. This is called post exposure prophylaxis (PEP), which is recommended that is started as early as possible in increase the chance of effectiveness. It is important to note that PEP involves taking HIV treatment medication for a whole month. This will have a lot of side effect and is also not guaranteed to work (Smith, Grohskopf & Black, et al. 2005)
Berhane, et al. (2004), observes that it is important that an individual who test positive of HIV have regular blood test done to monitor the progress of the virus even before treatment is started. This is because treatment is only recommended when the virus starts weakening the immune system. This is determined by measuring the level of the CD4, the infection fighting cells in the blood. Treatment is only begun when the CD4 counts go below 350. Treatment has been found to lower the level of HIV in the blood therefore reducing the chance of passing it over to another person.
There are many treatments available for the treatment of HIV although there is no complete cure yet. This has enabled people to live longer and healthier lives that before. The drugs available currently will not only slow the growth of virus but will also stop it from making copies and replicating in the body system (Lewin, et al. 2011). And even thought the drugs will not eliminate the drugs from the body system, the amount of the virus in the blood will be kept low. The amount of the virus in the blood known as viral load is measured by undertaking a test. The lower the viral load, the healthier a person is and the longer his body can fight off infections.
Background of treatment of HIV
Barlett, (2006), posits that the treatment of HIV started in 1987 with the introduction of the drug AZT that was approved to fight HIV. Since that time, many drugs have been researched and introduced into the market to be used. As a result, more than 30 drugs are now available to be used to treat people living with HIV and AIDS and more drugs are still under development.
Some of the popular drugs for treatment of HIV are ‘the cocktail”, Antiretroviral (ARVs) and Highly Active Antiretroviral Therapy (HAAT or ART). Quashie, Mesplède &Wainberg, (2013), submitted that the drugs used in the treatment of HIV have been classified into five different categories; each class of the drugs will affect the disease virus at different point of its life cycle. As a result, most of the HIV patient under medication will take three different drugs that are in two different classes (Cohen, et al. 2004). This regimen is the standard HIV treatment and that will be used to take care of the patients so as to increase the chances of getting the virus at one stage of its circle of development. This is also important because no drug has been proved to cure HIV or AIDS hence taking a single drug will not prevent one from the harm of the Virus. On the other hand, Bai, Xue, Wang, Cai, et al. (2013) contends that taking three different drugs of HIV is effective in controlling the amount of the virus in the body hence protecting the immune system of the patient. In addition, taking more than one drug will prevent the HIV patient from being resistant to the drug. The state of drug resistance occurs when the HIV reproduces itself through the process of mutation hence producing copies of it that are not perfect. These imperfect mutations are not able to respond to the drugs that are taken to control the HIV.
HIV medication and types of treatment classes
Each of the different drugs that are used to control HIV is very powerful by itself. The best strategy to treating the HIV successfully is in picking the right combination of the drugs to be taken from the different classes of HIV medicines.
The Antiretroviral are also separated into different classes by the way an individual drug ability to stop the HIV replication in the body. The classes are as follows:
Nucleoside or Nucleotide Reverse Transcriptase Inhibitors (NRTIs)
Wensing, Maarseveen, Nijhuis, (2010) indicate that this kind of HIV drugs are also called the ‘nukes’ because of the way they work to block a very important step in the HIV process of reproduction. The NRTIs work like faulty building blocks in the production of viral DNA cell. It therefore result in the blocking of the HIVs ability to use the special type of enzyme also called reverse transcriptase to correctly build the genetic material of the DNA that is required by the Virus to build its own copies.
Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs)
These are also called the non nukes but work in very similar way as the nukes. The Non nukes operate by blocking the enzyme process of reverse transcriptase and in the process preventing the HIV from making copies of its own DNA. But unlike the nukes which work on the genetic material, the NNRTIs works directly on the enzyme itself leading to prevent it from functioning correctly.
Protease Inhibitors (PIs)
Wensing, Maarseveen, Nijhuis, (2010) submits that these drugs work from the understanding how the HIV replicates itself inside the body cells. When the HIV replicates itself in the body cell, it first creates a very long strand of its own genetic material. For the HIV to make more copies of it, the long strands have to be cut into shorter strands. The protease is the enzyme that is used to cut up the long strands of the genetic material. The Protease Inhibitors also known as stoppers are therefore used to block this enzyme and effectively prevent the long strand from the genetic material from being cut up into functional pieces that will reduce the defense of the body systems.
Entry /Fusion Inhibitors
These types of HIV medications function by blocking the virus from entering the body cells from the start. The HIV virus needs a way to attach itself to the cells and therefore bond with the CD$ cells. The HIV does this through the special structure cells known as the receptor sites (Jain & Deeks, 2010). These receptor sites are found in both the CD4 cell where they exist in other types of cells too and the HIV cells. The Fusion inhibitors drugs will therefore work to target the sites on either CD4 or HIV so as to prevent the HIV from attaching itself to the healthy cells in the body.
Integrase Inhibitors
The HIV uses the body cells in the patients to make its own DNA through a process known as transcription. Once this has taken place, the virus will integrate into the genetic material in the cells of the patient. This process is done through an enzyme known as integrase. The integrase inhibitors drugs function by blocking this enzyme and therefore preventing the enzyme from adding to itself into the DNA and the CD4 cells. In this way, the virus is prevented from replicating itself in the cells (Bai, Xue, Wang, Cai, et al. 2013).
Fixed dose combinations
These are not really a separate group of HIV medication but a combination of the different classes that are mentioned in addition to other advanced HIV medicines. These are therefore antiretroviral that combine two or more medication from the different classes to come up with a single pill that has fixed doses of all the other drugs.
Which medication is right for a patient?
The medical provider will consider many factors when deciding which treatment drugs are suited for the patient. Some of the issues will involve the general state of your health that is determined by the CD4 count, side effects of the drug and the psychiatric history.
Sometimes the patient has to be provided with other medications in addition to the HIV treatment. Prophylaxis treatment may be prescribed to patients so as to prevent other opportunistic infections. The patient may need to take other drugs to prevent side effects like pain, nausea and diarrhea. Medications may also be given to treat other health problems like diabetes and high blood pressure (Cohen, Chen, McCauley et al. 2011).
The doctors and the nurses will also be observing the patients for other conditions that accompany the HIV infection. When a patient is diagnosed with hepatitis B or hepatitis C, it is always recommended that treatment is started when the CD4 count falls below 500. On the other hand, the patient on chemotherapy or radiotherapy is required to start the HIV treatment at any stage because these intensive treatments will suppress the immune system.
References
Bai, Y; Xue, H Wang, K Cai, L et al. 2013, “Covalent fusion inhibitors targeting HIV-1 gp41 deep pocket“. Amino Acids the Forum for Amino Acid, Peptide and Protein Research 44 (2): 70.
Barlett, JD., (2006). “Ten years of HAART: Foundation for the Future“. Medscape.
Berhane, K et al. (2004). “Impact of highly active antiretroviral therapy on anaemia and relationship between anaemia and survival in a large cohort of HIV-infected women: Women’s Interagency HIV Study“. Journal of Acquired Immune Deficiency Syndromes 37 (2): 1245–52. PMID.
Cohen, MH et al. (2004). “Medically eligible women who do not use HAART: The importance of abuse, drug use, and race“. American Journal of Public Health 94 (7): 1147–51.
Cohen, MS Chen,YQ McCauley, M et al. (2011). “Prevention of HIV-1 infection with early antiretroviral therapy“. The New England Journal of Medicine 365 (6): 493–505.
Jain, V & Deeks, SG (2010).”When to start antiretroviral therapy”. Current HIV/AIDS Reports 7 (2): 60–8.
Lewin, SR et al. (2011). “Finding a cure for HIV: will it ever be achievable?” AIDS 14 (4): 4. PMC.
Quashie, PK Mesplède, T Wainberg, MA (2013). “HIV drug resistance and the advent of integrase inhibitors“. Current Infectious Disease Reports 15 (1): 85–100.
Smith, DK, Grohskopf, LA, Black, RJ et al. (2005). “Antiretroviral post exposure prophylaxis after sexual, injection-drug use, or other nonoccupational exposure to HIV in the United States: Recommendations from the U.S. Department of Health and Human Services“. Morbidity and Mortality Weekly Report 54 (RR–2): 1–20.
Wensing, AM Maarseveen, NM Nijhuis, M (2010). “Fifteen years of HIV protease inhibitors: Raising the barrier to resistance“. Antiviral Research 85 (1): 59–74.
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