Human Immunodeficiency Disorder (HIV) Is A Viral Infection

Human Immunodeficiency disorder (HIV) is a viral infection. The infection

Human Immunodeficiency Virus (HIV) remains one of the most significant global health challenges, characterized by its ability to infect and deplete CD4+ T lymphocytes, critically impairing cell-mediated immunity. This compromised immune state increases vulnerability to various opportunistic infections and certain malignancies, ultimately leading to Acquired Immunodeficiency Syndrome (AIDS) if untreated. Understanding the pathophysiology, modes of transmission, clinical progression, and associated immune dysfunctions of HIV is essential in managing and preventing its spread.

HIV is a retrovirus with two primary types: HIV-1 and HIV-2, with HIV-1 being the most prevalent worldwide (Cachay, 2019). The virus is transmitted through contact with infected body fluids such as blood, semen, vaginal fluids, rectal secretions, and breast milk. Transmission routes include unprotected sexual contact, sharing contaminated needles, transfusion of infected blood products, and from mother to child during childbirth or breastfeeding. The virus primarily targets CD4+ T lymphocytes by attaching to the CD4 receptor and chemokine co-receptors on T cells, macrophages, and dendritic cells (Cachay, 2019). This binding facilitates entry of the viral RNA into host cells, initiating the infection process.

Upon entry, HIV reverse transcribes its RNA genome into DNA, which then integrates into the host cell genome. This process involves several viral enzymes including reverse transcriptase, integrase, and protease. The integrated provirus can either enter a latent state or replicate actively, producing new viral particles that bud from the host cell membrane. These mutations allow HIV to evade immune responses and develop resistance to antiretroviral therapy (Leonard et al., 2008). The continuous replication and mutation lead to the high genetic variability characteristic of HIV, complicating vaccine development and treatment efforts.

The clinical course of HIV infection involves distinct stages: acute infection, clinical latency, and AIDS. During acute infection, individuals often experience flu-like symptoms within days to weeks after exposure, such as fever, lymphadenopathy, sore throat, and rash, reflecting high viral replication and dissemination. This phase is followed by a prolonged asymptomatic period where the virus persists at lower levels in reservoirs, and the immune system partially controls viral replication. Without treatment, the disease progresses, and CD4+ cell counts decline steadily. When the CD4+ count falls below 200 cells per microliter of blood, the patient is diagnosed with AIDS, characterized by severe immunodeficiency and susceptibility to opportunistic infections and neoplasms (Cachay, 2019).

Laboratory diagnosis of HIV involves serological testing for HIV antibodies and p24 antigen detection, along with nucleic acid tests (NAT) for viral RNA. The CD4+ T cell count is a critical marker for assessing immune function and disease progression. A CD4+ count below 200/mcL is diagnostic of AIDS, and combined with clinical signs, indicates advanced immunosuppression. Regular monitoring of viral load—a measure of HIV RNA in the blood—is essential in evaluating treatment effectiveness and disease progression (Cachay, 2019).

Behavioral risk factors significantly influence the epidemiology of HIV. Men who have sex with men (MSM), particularly those engaging in anal-receptive intercourse, are at the highest risk due to the vulnerability of mucous membranes to viral entry (Cachay, 2019). Substance use, especially injection drug use, also contributes to transmission. Preventative strategies include safe sex practices, regular testing, pre-exposure prophylaxis (PrEP), and harm reduction approaches for drug users.

Management of HIV involves lifelong antiretroviral therapy (ART) aimed at suppressing viral replication, restoring and preserving immune function, and preventing disease transmission. These therapies target various stages of the viral life cycle, including reverse transcriptase inhibitors, protease inhibitors, integrase inhibitors, and entry inhibitors. Early initiation of ART has dramatically decreased AIDS-related morbidity and mortality, transforming HIV infection from a fatal disease into a manageable chronic condition (Fox & Isenberg, 2007). Adherence to therapy is critical to prevent resistance and ensure sustained viral suppression.

Systemic Lupus Erythematosus (SLE) and Its Immunopathology

In contrast to HIV, systemic lupus erythematosus (SLE) is an autoimmune disease characterized by immune system dysregulation leading to multi-organ tissue damage. SLE involves a loss of self-tolerance with activation of autoreactive T and B lymphocytes, resulting in the production of pathogenic autoantibodies, such as anti-dsDNA and anti-Smith antibodies, which deposit in tissues and incite inflammation (Choi, Kim, & Craft, 2012). The disease pathogenesis involves complex interactions among genetic predispositions, environmental factors, and immune abnormalities.

The primary targets of tissue injury in SLE include the kidneys, skin, joints, and the hematopoietic system. Renal involvement, manifesting as lupus nephritis, is a leading cause of morbidity and can result from immune complex deposition in glomeruli, triggering inflammatory responses. The inflammatory cascade involves cytokines like interferons and interleukins, which perpetuate immune activation and tissue damage (Choi et al., 2012). Immune cell infiltration, especially of T cells and B cells, amplifies this process, leading to the clinical features observed in active SLE.

CD4+ T lymphocytes play a crucial role in the pathogenesis of SLE, regulating B cell antibody production and infiltrating affected tissues. Unlike in HIV, where immune suppression occurs, in SLE, the immune system becomes hyperactive and attacks self-antigens. This overactivity results in increased inflammation, tissue destruction, and systemic symptoms including fatigue, fever, arthralgia, and skin manifestations. Laboratory findings often reveal elevated levels of autoantibodies, decreased complement components, and evidence of end-organ damage.

Despite their contrasting presentations, both HIV and SLE involve abnormalities in CD4+ T cell function, though their directionality differs. In HIV, there is a depletion of CD4+ T cells leading to immunodeficiency, while in SLE, the CD4+ T cells contribute to autoreactive immune responses causing tissue injury (Fox & Isenberg, 2007). Understanding these immunological mechanisms is vital for developing targeted treatments for both conditions.

Comparison of HIV and SLE

Both HIV and SLE significantly involve the immune system but in different ways. HIV causes immunosuppression by directly destroying CD4+ T cells, thereby impairing adaptive immunity and increasing susceptibility to infections. Conversely, SLE results from immune hyperactivation, with autoreactive lymphocytes attacking host tissues. These fundamental differences highlight distinct pathophysiological mechanisms despite overlapping features such as CD4+ T cell dysfunction.

Understanding the immune dysregulation in each disease facilitates tailored therapeutic strategies. ART effectively suppresses HIV replication, restoring immune function, whereas management of SLE primarily involves immunosuppressive agents like corticosteroids and disease-modifying antirheumatic drugs (DMARDs) to control autoimmunity (Choi et al., 2012). Continuous research is essential for further elucidating these mechanisms and improving patient outcomes.

References

• Cachay, E. R. (2019). Human Immunodeficiency Virus (HIV) Infection - Infectious Diseases.
• Choi, J., Kim, S. T., & Craft, J. (2012). Pathogenesis of systemic lupus erythematosus update. Pathology, 44. doi: 10.1016/s.
• Fox, R. A., & Isenberg, D. A. (2007). Human immunodeficiency virus infection in systemic lupus erythematosus. Arthritis & Rheumatism, 40(6). doi: 10.1002/art.
• Leonard, J. N., Shah, P. S., Burnett, J., C., & Schaffer, D. V. (2008). HIV Decades RNA Interference Directed at TAR by an Indirect Compensatory Mechanism. Cell Host & Microbe, 4(5). doi: 10.1016/j.chom.2008.09.008.
• What is lupus? (2019).