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AIDS is a medical condition. A person is diagnosed with AIDS when their immune system is too weak to fight off infections. In 1981 the first cases of AIDS were identified among gay men in the US. However, scientists later found evidence that the disease existed in the world as early as 1959. The first documented case of HIV was traced back to 1959 using preserved blood samples, which were analyzed in 1998. Acquired immunodeficiency syndrome, shortened AIDS, is caused by HIV. HIV affects the cell in such a way, that it begins to die-weakening the immune system. HIV provirus may lie dormant with in a cell for a long time. But when the cell becomes activated, it treats HIV genes in much the same way as human genes. There are two types of HIV: HIV-1 and HIV-2. Both types are transmitted by sexual contact, through blood, from mother to child and they appear to cause clinically indistinguishable AIDS. HIV-infected patients with weakened immune systems can develop life-threatening infections. The development of cryptosporidiosis, pulmonary and lymph node tuberculosis, wasting, persistent fever (longer than one month), persistent candidasis, recurrent bacterial pneumonia, and other opportunistic infections is common. These patients may be wasting or losing weight.

According to UNAIDS, there were approximately 37.9 million people across the globe with HIV/AIDS in 2018. Of these, 36.2million were adult and 1.7 million were children (<15years old). New HIV infection – An estimated 1.7 million individuals worldwide were newly infected with HIV in 2018.Blood coagulation abnormalities occur frequently in people infected with Human Immunodeficiency Virus (HIV). Researches so far shows the retrovirus is associated with endothelial dysfunction and liver damage. Both endothelial dysfunction and liver damage can result in coagulation defect because most coagulation factors are produced in the liver and some are activated by the tissues therefore default to them can lead to coagulation defect. It is therefore expected that as HIV progresses coagulation abnormalities increases. However, few studies showed the association of these abnormalities with antiretroviral therapy (ART). Prothrombin time (PT) and partial thromboplastin time with kaolin (PTTK) use to assess the extrinsic and intrinsic pathway respectively alongside with platelet count help to screen for coagulation abnormalities in HIV infected person. The intrinsic pathway comprising of factor I,II,IX,X,XI and factor XII while the extrinsic pathway comprising of factor I,II,V,VIII and factor X. HIV-related thrombocytopenia (Tr-HIV) is the most common haemostatic disorder with a high morbidity and affects patients from every risk group independently of age, sex, or stage of infection. Two mechanisms are responsible for the Tr-HIV: bone marrow failure and immunological disorders, namely, circulating immune complex deposited on the platelet membrane and the production of autoantibodies directed against platelets.

Human Immunodeficiency Virus (HIV) infection is a major public health threat to the existence of human beings especially to the developing countries like in Africa. Human Immunodeficiency Virus attacks the CD4 T cells thereby suppressing the immunity of the human host. There is high level of malnutrition in the developing countries due to poor economic status of many individuals with attendant immunodeficiency which affects the patients with HIV drastically for survival. Patients with HIV infection should maintain good nutritional status with improved immunity for increased life span and effectiveness in their works. A lot of commitment from the society is needed to encourage the patients with HIV to reduce the morbidity and mortality rates associated to HIV infection.

Sexually Transmitted Infections (STIs) remain a serious reproductive health problem globally. In Africa, the rate of infection of STIs among youth remains high and research shows that there is 45% rise in STI cases among youth aged 15 – 25 years. Similarly, although testing and treatment services for sexually transmitted diseases are provided at most health centers, the rate of STI infection among youth remains high. This was influenced by various factors including inadequate knowledge about the effective use of preventive measures such as condoms, gender roles, risky sexual practices such sexual networking, having multiple partners as well as misperceptions about condom use among others.

The human immunodeficiency virus (HIV) infection is one of the health burdens ravaging the world with severe impact in developing regions. Women and young girls are more threatened by HIV infection than their male counterparts. Notably, in 2022, 63% of all new HIV infections were attributed to women in sub-Saharan Africa. The anatomical architecture of the female genital tracts, poverty, gender imbalance, unrefined cultural norms aimed at subjugating women, early exposure to sex and marriage, and illiteracy are fingered to contribute to the increased risk of HIV infection in women and young girls. Mitigating these factors will no doubt help curb the prevalence of HIV infection. Herein, we highlighted some measures that could help turn down women’s risk of getting HIV including abstinence, regular use of condoms, delay in sexual exposure, maintaining one faithful partner, timely voluntary counseling and testing, formal education, monitoring of alcohol use, proper dieting, and scrapping of cultural norms targeted at subjugating women. Successfully turning down HIV infection risk in women and young girls will be a breakthrough in the combat against HIV infection since women and young girls being the most vulnerable group must have been salvaged. This paper reviewed the prevalence of HIV/AIDS in women and young girls, the factors fueling the high prevalence, and enumerated key areas to target in order to minimize this menace. Related published data from various databases were utilized.

Co-infection with both HIV and malaria presents a complex medical challenge, particularly concerning hematocrit variations that often result in anemia in affected individuals. This comprehensive review aims to explore and synthesize existing literature to elucidate the multifaceted nature of hematocrit alterations observed in HIV patients concurrently infected with malaria. The pathophysiological mechanisms contributing to hematocrit variations in this co-infected population involve a complex interplay between the immunosuppressive effects of HIV and the hemolytic nature of malaria parasites. Understanding these mechanisms is crucial for developing targeted interventions. Diagnostic challenges abound due to overlapping symptoms and limitations in conventional diagnostic tools, necessitating the exploration of more advanced diagnostic methodologies to accurately assess and monitor hematocrit levels in co-infected individuals. The clinical implications of hematocrit variations in this context extend beyond mere anemia, impacting disease severity, treatment response, and the overall prognosis of affected patients. Anemia complicates therapeutic interventions, potentially affecting the efficacy of antiretroviral and antimalarial treatments. Persistent anemia in co-infected individuals increases vulnerability to opportunistic infections and compromises treatment outcomes, underscoring the necessity for comprehensive management strategies. These strategies encompass a holistic approach involving antiretroviral therapies, antimalarial drugs, nutritional support, and potential interventions such as blood transfusions in severe cases. In conclusion, this review consolidates current knowledge, emphasizing the need for further research to elucidate the nuances of hematocrit variations in HIV patients co-infected with malaria. Improved understanding, enhanced diagnostic modalities, and optimized management strategies are crucial to mitigate the impact of anemia and improve outcomes in this vulnerable patient population.

Co-infection with HIV and malaria presents a multifaceted clinical scenario with intricate immunological interplays, wherein neutrophils, the primary mediators of innate immunity, emerge as pivotal actors. This paper aims to comprehensively analyze the dynamic role of neutrophils in the progression of HIV within the context of malaria co-infection. Neutrophils, conventionally viewed as short-lived effectors, exhibit remarkable plasticity and multifunctionality, contributing significantly to immune responses during co-infections. Their phenotype and functions undergo profound alterations in response to the complex milieu of both HIV and malaria, impacting disease progression and immunomodulation. This paper scrutinizes the nuanced alterations in neutrophil phenotypes, their diverse effector functions, and their contributions to immunopathogenesis within the HIV-malaria co-infection paradigm. Neutrophils, driven by dysregulated cytokines and inflammatory cues, exhibit heightened activation, potentially exacerbating tissue damage and chronic immune activation. Insights gleaned from understanding neutrophil dynamics in this co-infection scenario hold significant therapeutic implications. Potential interventions targeting neutrophil responses offer promising avenues for modulating immune dysregulation and managing disease progression. The review underscores the need for innovative therapeutic approaches aimed at harnessing neutrophil functionalities to mitigate HIV progression within malaria co-infected individuals. In conclusion, unraveling the intricate roles of neutrophils provides critical insights into the immunopathogenesis of HIV within the context of malaria co-infection. This comprehensive understanding not only sheds light on immune modulation but also presents a foundation for future therapeutic strategies aimed at improving clinical outcomes in this complex co-infection scenario.

Anemia remains a prevalent complication in individuals living with Human Immunodeficiency Virus (HIV), exerting a significant impact on disease progression and patient prognosis. Platelet Distribution Width (PDW), an established measure reflecting platelet heterogeneity, has garnered attention as a potential prognostic marker for evaluating anemia severity in this patient population. This review provides a comprehensive analysis of the utility of PDW in prognosticating anemia severity in HIV patients, aiming to explore its clinical relevance, associations, and implications for disease management. The prevalence of anemia in HIV patients is discussed, emphasizing its multifactorial etiology and adverse effects on the overall health and prognosis of affected individuals. The introduction outlines the necessity for reliable prognostic indicators to assess anemia severity in the context of HIV and sets the stage for evaluating PDW as a potential solution. In conclusion, this review highlights the potential of PDW as a valuable prognostic marker for evaluating anemia severity in HIV patients, underscoring its potential impact on disease management and the need for continued research to validate and incorporate PDW measurements in routine clinical practice.

Platelets, conventionally recognized for their pivotal roles in hemostasis and thrombosis, have emerged as multifunctional players in immune responses. In the context of Human Immunodeficiency Virus (HIV) infection, platelets exhibit intricate interactions influencing viral pathogenesis, immune activation, and disease progression. This review aims to provide an in-depth analysis of the diverse roles played by platelets in modulating HIV infection, shedding light on their impact on viral dynamics, immune responses, and associated pathophysiological processes. The paper addresses platelet-driven alterations in coagulation pathways and endothelial function in the context of HIV, emphasizing their role in HIV-associated coagulopathies, endothelial activation, and consequent vascular dysfunction. Additionally, the involvement of platelets in the development of HIV-associated comorbidities such as cardiovascular complications, neurocognitive impairment, and systemic inflammation is discussed, delineating platelet-driven mechanisms contributing to the pathogenesis of these conditions and their implications for disease outcomes. In conclusion, the multifaceted roles of platelets in HIV infection underscore their significance beyond hemostasis, offering potential insights into therapeutic avenues and highlighting the need for further investigations to decode the complexity of platelet-driven modulation of HIV infection.

The management of Human Immunodeficiency Virus (HIV) necessitates a nuanced comprehension of immune responses, with the CD4/CD8 ratio emerging as a pivotal parameter in this regard. This review investigates the clinical implications of CD4/CD8 ratios in HIV, encompassing their role as prognostic markers, treatment monitoring tools, and indicators of immunological reconstitution during antiretroviral therapy. We explore the baseline CD4/CD8 ratio in healthy individuals, scrutinize its prognostic significance in HIV progression, and assess its dynamic changes throughout treatment. Additionally, the article addresses challenges, controversies, and future directions in CD4/CD8 ratio research, offering a comprehensive overview of its potential as a key immunological marker in the ongoing battle against HIV.

This review article provides an in-depth exploration of the current trends and challenges associated with blood transfusion practices in individuals living with HIV. As advancements in antiretroviral therapy (ART) have significantly improved the life expectancy of HIV-positive individuals, the landscape of blood transfusion strategies and safety considerations has evolved. The review delves into key trends, including personalized transfusion approaches, hemovigilance systems, and innovations in blood screening technologies. Additionally, it addresses challenges such as potential interactions between blood transfusion and antiretroviral medications, the impact on viral load dynamics, and emerging infectious risks. By synthesizing existing literature, this review aims to provide insights that guide healthcare professionals in optimizing blood transfusion practices for individuals with HIV while addressing the unique challenges posed by this patient population.

The immune response against human immunodeficiency virus (HIV) infection is a complex interplay between various components of the immune system, with CD8+ T-cells occupying a central role in viral control. This review critically examines the functionality of CD8+ T-cells in HIV defense, highlighting their importance in controlling viral replication, the evasion strategies employed by HIV, and the challenges encountered in harnessing CD8-mediated immunity for therapeutic purposes. We discuss the heterogeneity of CD8+ T-cell responses, the mechanisms of viral escape, and the phenomenon of CD8+ T-cell exhaustion. Additionally, recent advancements and controversies in the field are addressed, along with future perspectives on enhancing CD8-mediated immunity as a therapeutic strategy against HIV. This review aims to provide a comprehensive understanding of the complexities surrounding CD8+ T-cell functionality in HIV defense, paving the way for further research and therapeutic developments in the fight against HIV/AIDS.

Antiretroviral therapy (ART) has revolutionized the management of human immunodeficiency virus (HIV) infection, significantly reducing morbidity and mortality rates worldwide. However, emerging evidence suggests that ART may be associated with alterations in platelet function and homeostasis, leading to platelet aberrations such as thrombocytopenia and platelet hyperactivity in HIV patients. This review provides a comprehensive overview of the relationship between ART and platelet aberrations in HIV-infected individuals. We discuss the epidemiology, pathogenesis, clinical manifestations, and management strategies of platelet abnormalities associated with ART, including immune reconstitution inflammatory syndrome (IRIS)-related thrombocytopenia and ART-induced coagulation disorders. Furthermore, we explore potential mechanisms underlying ART-induced platelet aberrations, including direct drug toxicity, immune-mediated mechanisms, and viral factors. Understanding the impact of ART on platelet function and homeostasis is essential for optimizing the management of HIV-infected individuals and minimizing the risk of associated complications.

Early Infant Diagnosis (EID) plays a crucial role in ensuring a HIV-free start for newborns born to HIV-positive mothers. This review highlights the significance of EID in pediatric HIV care, emphasizing its role in timely identification of HIV infection, prevention of morbidity and mortality, facilitation of Prevention of Mother-to-Child Transmission (PMTCT) programs, reduction of HIV transmission, and promotion of long-term health outcomes. Despite its importance, EID faces challenges such as limited access to testing services and logistical constraints. Addressing these challenges requires strengthening health systems and leveraging innovative approaches to expand access to EID services. Investing in EID programs is essential for achieving global HIV elimination targets and advancing towards an AIDS-free generation.

Antiretroviral therapy (ART) has revolutionized the management of HIV infection, significantly reducing morbidity and mortality in individuals living with the virus. However, the influence of ART on maternal eosinophil levels during pregnancy remains a topic of interest and debate. This review explores the current understanding of how ART affects eosinophil levels in pregnant women living with HIV, considering both the potential mechanisms underlying these changes and their clinical implications. Keywords such as HIV, antiretroviral therapy, pregnancy, eosinophils, immune response, and maternal health are utilized to delve into relevant literature and provide insights into this complex interaction. Understanding the impact of ART on maternal eosinophil levels can contribute to optimizing the management of HIV during pregnancy, ensuring maternal health, and promoting favorable pregnancy outcomes.

Hematologic complications represent a significant burden in individuals living with Human Immunodeficiency Virus (HIV) infection, with anemia being one of the most prevalent and clinically relevant manifestations. Central to the pathophysiology of HIV-associated anemia is the dysregulation of erythropoietin (EPO), the principal hormone governing red blood cell production. This review examines the intricate interplay between HIV infection and erythropoiesis, focusing on the mechanisms underlying EPO dynamics. Chronic inflammation, cytokine dysregulation, and direct viral effects disrupt the delicate balance of EPO regulation, leading to impaired erythropoiesis and anemia. Moreover, antiretroviral therapy (ART) may exert additional effects on EPO synthesis and hematopoiesis. Understanding these dynamics is crucial for devising effective therapeutic strategies tailored to individual patient needs. Future research endeavors should aim to unravel the complex pathways governing EPO regulation in HIV infection, paving the way for personalized management approaches aimed at alleviating anemia burden and improving patient outcomes.