HIV and How It Affects the Body

Acquired Immunodeficiency Syndrome (AIDS) is a longstanding viral infection caused by the Human Immunodeficiency Virus (HIV). It is characterized by the destruction of T-helper cells in the immune system, thus rendering an individual susceptible to opportunistic infections (VanMeter & Hubert, 2014). AIDS is an infectious disorder that is disseminated by exposure to infected body fluids such as blood, seminal and vaginal fluids through sexual intercourse, cuts, blood transfusion, or from mother to child during childbirth. The purpose of this paper is to describe the pathophysiology of HIV, its diagnosis, different stages of the disease, treatment modalities, and how they work on the human body. A prognosis of the disease is also provided.


HIV is a retrovirus containing RNA. It falls under a group of viruses known as lentiviruses because they take time to develop active disease. Two main types of viruses exist HIV-1 and HIV-2. Both viruses are thought to have originated in Central Africa between 1894 and 1924 from chimpanzees that were hunted and eaten.

The HIV consists of two strands of RNA, a reverse transcriptase enzyme, and a lipid envelop with glycoproteins used to anchor to human cells. The binding of the virus to a T-helper cell permits the RNA and enzyme to enter the host cell. The virus uses the enzyme to convert the RNA to DNA through the process of reverse transcription. The viral DNA joins the CD4 cell’s DNA and redirects it to synthesize viral constituents, which assemble to form new viruses, leading to the replication of the virus.

The infected T-helper cell releases many viruses and is in turn destroyed. Therefore, the virus attacks CD4 (T-helper lymphocytes) and reduces their numbers, which impairs humoral and cell-mediated immune responses. The virus also affects macrophages and cells of the central nervous system. In the early phases, the virus replicates in the lymphoid tissues such as the tonsils, lymph nodes, and spleen.


HIV is diagnosed by detecting antibodies against it in blood using an immunoassay known as enzyme-linked immunosorbent assay (ELISA). Rapid diagnostic tests can ascertain the presence or absence of infection within 15 to 20 minutes. Noninvasive testing that uses saliva instead of blood can still be used. The disorder can also be diagnosed using more accurate techniques such as polymerase chain reaction (PCR), which detects the virus DNA or RNA in blood or body fluids. An HIV-positive person has the virus in their body while an HIV-negative individual does not have the virus in their system.

AIDS is diagnosed based on the number of CD4 cells in the blood, which should be less than 200 cells per cubic milliliter of blood (VanMeter & Hubert, 2014). However, in the absence of sophisticated diagnostic equipment to measure the CD4 count, a diagnosis of AIDS is made based on the appearance of opportunistic diseases such as Kaposi’s sarcoma, pneumonia, and weight loss.


HIV infection has three main stages of seroconversion, latent period, and active disease. The seroconversion stage, which is also referred to as the window period, is the time between infection and the development of antibodies against the disease. At this point, HIV is in the body, even though antibodies against it are yet to be developed. Mild symptoms such as flu-like indications may be present (Avert, 2019). This phase lasts from 2 to 10 weeks.

The latent period is the time between seroconversion and manifestation of disease symptoms during active infection. This period can last many years or decades depending on the viral load (viremia) and concentration of normal CD4 cells. During this period, the body develops many antibodies against HIV. Small quantities of the virus can be found in the body as much as the symptoms of active disease are absent.

The active disease stage occurs when the number of healthy CD4 cells declines, rendering the body susceptible to opportunistic infections. The viral load also increases together with HIV antibodies. This phase is characterized by indications such as wasting syndrome, lymphoma, dementia, and specific opportunistic diseases.


HIV does not have a cure. However, antiviral medications can minimize the replication of the virus. Different drugs target various stages of the virus’s life cycle in a human host. Protease inhibitors (PIs) are a group of drugs that impede viral protein synthesis. It includes medications such as ritonavir, saquinavir, and lopinavir (Sampson et al., 2019).

Entry inhibitors such as maraviroc prevent the multiplication of the virus by impairing the entry of viral proteins into uninfected T-helper cells. Fusion inhibitors, conversely, hamper the merging of the viral and healthy host cell membrane during the early stages of infection. An example of a fusion inhibitor is enfuvirtide.

Integrase strand transfer inhibitors (INSTIs) are medications that interfere with the incorporation of the viral DNA into the host cell DNA. A well-known example is a raltegravir. Three to five medications from different categories may be used simultaneously to extend the latent phase and reduce the viral load during active infection.


People with untreated HIV can live for several years before developing active disease. However, with proper care and consistent antiretroviral therapy, a person with positive HIV can live for several decades. The prognosis can be enhanced by initiating treatment during pregnancy, the manifestation of severe indications, or during treatment for hepatitis B or kidney disease (Tenforde, Walker, Gibb, & Manabe, 2019).


HIV is an incurable infection that destroys the immune system and increases the body’s predisposition to opportunistic infections. However, the period between infection and active disease can be protracted using antiviral treatment. Knowledge of the virus’s life cycle is crucial to the development of effective antiviral agents.


Avert. (2019). Symptoms and stages of HIV infection. Web.

Sampson, M. R., Cao, K. Y., Gish, P. L., Hyon, K., Mishra, P., Tauber, W.,… Younis, I. R. (2019). Dosing recommendations for quetiapine when coadministered with HIV protease inhibitors. The Journal of Clinical Pharmacology, 59(4), 500-509.

Tenforde, M. W., Walker, A. S., Gibb, D. M., & Manabe, Y. C. (2019). Rapid antiretroviral therapy initiation in low-and middle-income countries: A resource-based approach. PLoS Medicine, 16(1), e1002723. Web.

VanMeter, K. C. & Hubert, R. J. (2014). Gould’s pathophysiology for the health professions (5th Ed.). St. Louis, MO: Elsevier.