Acquired Immune Deficiency Syndrome (AIDS) was initially acknowledged as a novel disease in 1981. The disease was recognized after a growing number of young homosexual men were reported to succumb to rare unscrupulous infections and unusual malignancies. Subsequently, a retrovirus currently regarded as human immunodeficiency virus type 1 (HIV-1) was identified as the contributing agent of what turned out to be the most overwhelming infectious disease to have appeared in the modern history (Sharp & Hahn, 2011, p.1). HIV clinical presentation is regarded to be complex since the description of AIDS in 1981. The disease can manifest in different ways based on the affected organs and simultaneous infections prevalent in the region. The first clinical presentation might mimic symptoms of the usual endemic disease in that specific region. Nevertheless, the manifestation severity relies on the health status baseline of the infected person. The most essential early HIV manifestation in Africa was patent by slim diseases such as wasting and diarrhea, dermatological symptoms, tuberculosis, fever, weight loss, and different opportunistic infections. Apart from tuberculosis that continues to rise, other AIDS-associated diseases are reducing gradually as a result of extensive application of opportunistic infections (Boniphace et al., 2011, p. 9). Other commonly reported symptoms according to Vogl et al. (1999, p.256) include cough, dry mouth, asthenia, pain, shortness of breath, and anorexia. HIV/AIDs is also associated with psychological symptoms that include worrying, feeling nervous, lack of energy, difficulty sleeping, feeling sad, feeling irritable, feeling drowsy, difficulty concentrating.
HIV-1 has a complex life cycle and its outcome and duration are reliant on the type of the target cell and cell activation. In the initial stages, HIV-1 gains cells access without triggering immediate fatal damages though the entry process can arouse intracellular signal forces that consequently may enhance viral replication. According to Simon, Ho, and Karim (2006, p.491), the two molecules on the envelope of HIV-1 that include the transmembrane protein (gp41) and the external glycoprotein create the spikes on the surface of the virion. In the process of entry, gp120 gets attached to the cell membrane by binding to the CD4+ receptors first. Later connections between chemokine co-receptors and viruses activate permanent conformational modifications. The actual fusion occurrence happens within minutes by the formation of pore and releases of the viral center onto the cytoplasm of the cell. The center stripping of the core is followed by the reverse transcription of the viral genome into DNA via the reverse transcriptase enzyme of the virus. During this process, association though different viral alternatives can be created because reverse transcriptase is prone to error and does not contain proofreading activity (Simon, Ho & Karim, 2006, p. 491).
At the infection midpoint, the host DNA repair enzyme together with viral protein integrase introduces the viral genome into gene-rich. The lens epithelium-derived froth factor (LEDGF/p75) which is a binding host factor for integrase enhances integration that marks the defining moment by permanently changing the cells into a possible producer of the virus. In the last stages, the creation of viral particles needs virus motivated and host motivated transcription. Viral proteins assembled in proximity and transported to the cell membrane. Virus outlet is none lytic and exploits the vesicular sorting path that usually mediates the endosomes budding into multivesicular bodies. HIV-1 gets access to this protein-ordering pathway by binding TSG101 through its late domain, a small sequence motif in Gag p6. The Gag-Pol poly-protein cleavage through the viral protease produces developed infectious virions (Simon, Ho & Karim, 2006, p. 491).
The HIV pathogenesis according to Calles, Evans, and Terlonge (n.d., p12) is primarily a struggle between the patient immune response and HIV replication, through immune-mediated and cell-mediated reactions. The HIV viral overload mediates the destruction of CD4+ T-cell indirectly or direct. Mature CD4+ cells are destroyed. These include CD4+ cells in the nervous system for instance microglia, bone marrow CD4+ progenitor cells, peripheral lymphoid organs, and the thymus. This destruction results in T-cell production failure and ultimate immune suppression. According to Calles, Evans, and Terlonge (n.d., p12), there are various CD4+ cell depletion mechanisms by HIV infection. The direct effect of HIV-mediated cytopathic includes syncytium formation or cell fusion and single-cell killing. The syncytium regards a multiple uninfected CD4+ cell fusion with a single HIV-infected CD4+ cell through interaction with CD4-gp120. This fusion yields to a giant cell or multinucleated syncytium that might eventually serve as a way to create more virions. The natural immune responses of the host also participate in CD4+ cell depletion, mostly via natural killer cells, cytotoxic CD8+ T-cells, and cellular cytotoxicity. Other techniques include programmed cell death also known as apoptosis, autoimmune killer cells, T cells superantigen-mediated activation, and anergy (Calles, Evans & Terlonge, n.d., p12).
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Physical examination is one clinical routine that is used to identify some of the guiding symptoms in disease diagnosis. According to Amsterdam et al. (2017, p.4), HIV-infected patients need routine physical assessment, to determine new development. Normally, there are no static kinds of signs or symptoms to be identified in HIV patients. However, there could be some physical body changes that can act as guidance. Some of the positive physical examination findings include hypertension, lipodystrophy, and lymphadenopathy, which are found to be non-malignant. Other positive physical examination findings include an enlarged prostate, gingivitis, anal skin tags, poor dental condition, simple common skin lesions, incisional hernia, and eczematous. Candida infection in the mouth is another common physical examination result characterized by white plague on the gum, tonsil, or the tongue (Amsterdam et al., 2017,p.4).
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HIV infection is recognized either by showing the virus presence through nucleic acid discovery using p24 antigen testing, polymerase chain reaction (PCR), or by culturing by growing the virus in cell culture, though in rare cases. HIV infection can also be diagnosed by detecting specific HIV antibodies in plasma or serum. The most frequently used test to identify HIV infection is antibody testing. According to Fearon (2005, p.25), seroconversion can be identified after the first two weeks of infection in most cases, due to the availability of highly sensitive HIV-1/HIV-2 enzyme immunoassay (EIA) test in the market today. The p24 antigen might turn positive before the detectability of antibodies in a minute number of early seroconverters that ate still in the window period. Thus to allow the laboratory to choose suitably testing, it is essential to offer a clinical history that includes symptoms or signs that align with seroconversion illness or recent high-risk behavior. All HIV diagnostic laboratories repeatedly confirm positive EIA screen tests with a different assay. According to Fearon (2005, p.25), the Western blot is a highly precise immunoblot that permits for the antibodies visualization to the HIV structural polypeptides.
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Radiommunoprecipation assay might be used by some laboratories as part of the HIV testing algorithm or as a confirmatory assay. In this particular assay test, the serum of the patient is reacted with radiolabelled viral proteins to create radioactive antigen-antibody complexes. In a situation where antibody testing might be inadequate to establish if a patient is infected, it is important to conduct DNA PCR, a method of nucleic acid amplification that permits the identification of viral DNA assimilated into the genomic DNA of the host cell. PCR is specifically helpful in testing infants born of HIV-positive mothers. It helps diagnose patients that are agammaglobulinemia or where patients seem to demonstrate advanced HIV infection symptoms but without demonstrating specific HIV antibodies. Other than diagnostic testing of HIV, laboratories might also provide quantitative PCR (RNA) testing to determine the viral load. This test is used to assist in determining drug therapy initiation and monitoring therapy effectiveness. Fresher patient management; HIV genotyping is also being used to help in tracking the drug resistance development and guide the antiretroviral drug selection modification (Fearon, 2005, p.26).
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The HIV infection contains extremely complex pathogenesis and substantially differs in various patients. Thus, it can be regarded as a very host-definite infection. The pathogenesis specificity of the disease normally complicates treatment choices that are currently accessible for HIV infection. Nevertheless, effective HIV infection management is probable using various combinations of accessible drugs. This treatment technique is collectively regarded as antiretroviral therapy (ART). According to Bhatti, Usman, and Kandi, (2016, p.5), standard ART is consists of a combination of not less than three medicines regarded as highly active antiretroviral therapy (HAART). Mostly, effective ART assists in controlling HIV multiplication in infected individuals and augment the CD4 cells count. This helps in delaying the asymptomatic infection phase, slowing the disease progression. It also assists in reducing transmission risks. According to Bhatti, Usman, and Kandi, (2016, p.6), the latest recommendation for ART by WHO includes the first-line ART that focuses on treating adults with a single NNRTI and two NRTIs. They includes efavirenz (EFV) + emtricitabine (FTC), or Lamivudine (3TC) + Tenofovir disoproxil fumarate (TDF) as a fixed-dose. In case of contradiction, FCT or 3TC+ TDF+ nevirapine (NVP), or 3TC +zidovudine (AZT) + NVP, or AZT+EFV+3TC can be used. If the first-line ART treatment fails, a second line can be used. This combines a ritonavir-boosted PI and NRTIs (Bhatti, Usman & Kandi, 2016, p.6).
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HIV is a life-long infection that cannot be treated completely but can be managed to ensure low virus count and improvement of CD4 cells in the patient body. With early diagnosis and proper ART therapy, an HIV patient has a chance of prolonging the asymptomatic infection phase that results in AIDS and ultimate death. A patient has a chance of living for up to five decades with the disease, especially when proper management is employed. However, when no treatment is offered, the patient is likely to turn asymptomatic within ten years after the infection and to succumb from the disease within three years after reaching the asymptomatic stage (Nettleman, 2019).
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Based on the analysis, HIV is a complex disease with an individual based clinical presentation based on the level of the immune system and the region. It also has a complex pathophysiology that makes it hard to address the disease. Once infected, the patient has to accept his or her status and live with the disease through proper disease management through ART therapy. When effectively managed a patient can live for decades and live a normal life. However, if ignored, the patient is likely to die within a decade. It is therefore important for a person to ensure early testing and diagnosis, when one is exposed to high virus risk or when one has a medical history demonstrating exposure to the virus. Early start of the disease management increase chances of controlling the viral load and improving CD4 counts easily. However, where possible, people should focus on employing preventive measures to avoid a lifetime struggle with the disease.
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