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HIV/AIDS

HIV/AIDS

Case Study: HIV/AIDS

Pathology of the Disease

            HIV infection begins without symptoms or ill-feeling. This process is accompanied by slight changes in the immune system. The stage spans up to three months following infection until seroconverson takes place, the process by which HIV-related antibodies can be detected by individuals after recent exposure (Naif, 2013). The impacts of infections and length of the disease progression with clinical symptoms usually differ widely from one person to another. However, it is usually a gradual process. Seroconversion may take many years to transition from primary infection to the ultimate development of symptoms of advanced HIV.

 During primary infection, while the patient may appear healthy, the virus actively replicates within the lymph nodes and blood stream of the infected person. As a consequence, the immune system can be vulnerable to other opportunistic infections. Examples of these infections may include Pneumocystis carinni, candidacies, Mycobacterium avium, as well as Mycobacterium tuberculosis. It is widely acknowledged that the infected persons usually develop AIDS when their plasma HIV viral load is high (Naif, 2013). During this phase, the CD4+ T count is usually less than 200 mm3. Nonetheless, the presence of highly active antiretroviral therapy may generate the dilemma on whether everybody who sereconverts to HIC will develop AIDS. One of the ways in which HIV debilitates the immune system is through infecting and destroying the CD4+ T cells. The process of weakening such cells results in immunodeficiency at latter phase of the disease. HIC usually adheres to the surface of CD4+ proteins in a manner that is sufficient to give room for entry. Nonetheless, the availability of CD4+ molecules along is sufficient proof not to allow the viral entry into other cell forms such as monocytes and dendric cells. As such, a second pathway is often required to gain access to infect cells (Naif, 2013). This phenomenon results to the identification of chemokine receptors, which are basic coreceptors for hiv-1.

Diagnosis and Laboratory Findings

            The diagnosis procedure for HIV is founded on the identification of specific antibodies, antigens, and both. From a laboratory perspective, there are numerous types of commercial kits, which are utilized to diagnose the infection. Serological tests are the most common methods that are utilized for screening (Davis et al. 2013). In the recent times, the advent of the rapid HIV-1 antibody tests has radically transformed the process of diagnosis. These tools and tasks are easy to perform and they generate findings within 20 minutes of undertaking the tests. Moreover, they allow for specimen gathering and effective diagnosis upon a single visit. Rapid tests are resourceful instruments for undertaking surveillance, screening, and diagnosis. They can be reliably undertaken on plasma, serum, entire blood and saliva by healthcare professionals. For the sake of staging, assessment of CD4+ cells and viraemia are needed (Davis et al. 2013). Plasma viral load is broadly utilized for the monitoring of therapeutic success on antiretroviral treatment. Various tests offer sensitive process of quantifying plasma HIV-RNA copies. Although the viral load can be used to determine the pace at which the immune system is being destroyed, the number of CD4+ cell cells often reveals the extent to which the patient suffers from immunodeficiency. Therefore, this tool is utilized to evaluate the phases of infection.

Signs and Symptoms

            There are no signs and symptoms that are distinct to HIV/AIDS. Therefore, the best way for determining HIV is to go for a test. HIV virus spreads via body fluids that attack the human’s immune system. Most People who have HIV may not feel sick for a long time. Nonetheless, HIV infection can lead to various symptoms, which vary depending on how long a patient has been infected. For many patients, flu-like symptoms often develop a few weeks after infection. These symptoms are characterized by fever, sore throat, as well as swollen glands in the neck. Since the disease damages the immune system, the patient develops other complications during the later stages of HIV. During that time, opportunistic infections that become common include Tuberculosis, Pneumositis, Kaposi Sarcoma, as well as candidiasis.

Genetic Component to the Disease

            HIV/AIDS is not a hereditary disease. However, genetic factors may play a significant role in determining HIV vulnerability. Genetic factors also influence mother-to-child-transmission and the progression of the disease. Out of these common genetic mediators, those that impact innate and adaptive immune system often seem to play a major role in the viral infectivity and pathogenesis. For instance, during primary infection, CCR5-utilizing virus is predominantly transmitted. Thus, polymorphisms that adversely affect the expression of CCR5 may alter the mother to child transmission and the rate of the disease progression.

Treatment

            Antiretroviral treatment provides the best option for long-lasting viral suppression and, consequently, reduction of morbidity and mortality. Nonetheless, recent drugs do not eliminate the HIV-1 infection; therefore, lifelong treatment is often required (Davis et al. 2013). Approximately 20 out of 21 antiretroviral drugs have been approved by the US food and Drug Administration (FDA). These drugs usually target the viral reverse transcriptase or protease. Eight nucleoside or nucleotide analogues and three non-nucleoside reverse transcriptase inhibitors often inhibit the process of viral replication after cell entry before integration (Davis et al. 2013). The utilization of fixed-dose combination tablets eases the treatment regiments through minimization of the daily pill burden.

References

Davis, D. H., Smith, R., Brown, A., Rice, B., Yin, Z., & Delpech, V. (2013). Early diagnosis and

treatment of HIV infection: magnitude of benefit on short-term mortality is greatest in

older adults. Age and Ageing42(4), 520-526.

Naif, H. M. (2013). Pathogenesis of HIV infection. Infectious Disease Reports5(Suppl 1).

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