_______________________________________________________________________ HIV/AIDS: An Update
• By region, the prevalence rates are nearly 40% higher in the Northeast and South (513.2 and 533.9 per 100,000, respectively) than in the West (379.7 per 100,000) and Midwest (263.6 per 100,000). • By race/ethnicity, 40% are Black/African American, 28% White, 26% Hispanic, 5% are multiracial, less than 2% are Asian/Pacific Islander, and less than 0.5% are American Indian/Alaska Native. • By age, the highest rate is seen in those 55 to 64 years of age (25%), followed by 45 to 54 years (21%), 35 to 44 years (20%), 25 to 34 years (18%), ≥65 years (13%), and 13 to 24 years (3%). • By sex at birth, 78% of adults and adolescents living with HIV are male. • By transmission category, 60% of HIV infections are related to male-to-male sexual contact, followed by heterosexual contact (25%), injection drug use (10%), and combined male-to male sexual contact and injection drug use (5%). Among HIV transmission by heterosexual contact, nearly 70% of all individuals infected are female. In 2022, an estimated 31,800 individuals 13 years of age or older were newly diagnosed with HIV/AIDS in the United States. United States incidence trends mirror those of the prevalence trends of HIV, with the exception of regional demographics [8].
Infected dendritic cells then fuse with CD4+ T lymphocytes and the infection extends to deeper tissue and, shortly there- after, to regional lymph nodes [12]. Within days, this prolif- eration of infected CD4+ T lymphocytes, combined with the migration of infected macrophages, leads to the appearance of viral RNA in the blood stream. This is followed by widespread secondary amplification of infection within the lymphoid tissue of the gastrointestinal tract, spleen, and bone marrow. Once the virus enters the cell, it may replicate, induce cell fusion and propagation of infection, or lead to cell death [12]. HIV targets the immune system, and the defining characteristic of HIV disease is progressive immunodeficiency caused by ongoing viral replication and cell-to-cell transmission within lymphoid tissue. With chronicity there is a progressive deple- tion of CD4 (helper-inducer) lymphocytes, the very T lympho- cyte cohort whose function it is to direct other cells in the immune system, and to orchestrate the inactivation of virus antigen. The result is a depressed T lymphocyte functional capacity, characterized by depletion of helper T cells (T4), impaired killer T cell activity, and increased suppressor T cells (T8). Eventually, impaired immunity renders the individual vulnerable to opportunistic infection and certain malignan- cies. The common laboratory measure of immune function is the CD4 cell count. In persons with intact lymphocyte immune systems, the normal number of CD4 T cells ranges from 600–1,200 cells/mcL, depending on the stage and dura- tion of infection. CLINICAL MANIFESTATIONS AND DISEASE COURSE The clinical manifestations of HIV disease are determined by the stage of primary infection and the chronicity and degree of the resultant cellular immunodeficiency state. Acute primary HIV infection may be asymptomatic, but most often it is manifest by a subacute viral syndrome of malaise and fatigue, fever, sore throat, rash, myalgia, headache, and lymph- adenopathy—clinical features similar in many respects to that seen with Epstein-Barr virus mononucleosis, cytomegalovirus (CMV), and certain types of herpes simplex infections [12]. A variety of atypical symptoms and signs may be seen, including aseptic meningitis syndrome, genital ulcers, and ulcerations involving the gingiva, palate, or buccal mucosa. Acute primary HIV illness usually resolves in less than 14 days but may follow a protracted course over many weeks [12]. Early in the chronic phase of HIV infection, when the CD4 lymphocyte population is only modestly depressed and declin- ing slowly, patients are often asymptomatic or may exhibit generalized lymphadenopathy and recurrent oropharyngeal candidiasis (thrush). During this stage, a reservoir of HIV is established throughout the lymphoid tissue system, includ- ing the spleen. Gradually, wandering (infected) macrophages disseminate the virus to certain internal organs, notably the brain, kidney, and adrenal glands.
A BRIEF OVERVIEW OF HIV DISEASE
VIRAL PATHOGENESIS HIV, known formerly as human T cell lymphotropic virus (HTLV-III), is a member of the retrovirus group and as such carries a ribonucleic acid (RNA) genome and a reverse tran- scriptase enzyme (RNA-directed DNA polymerase) that enables the virus to replicate within infected host cells. Susceptibility in humans is determined by the binding affinity of virion envelope proteins for a specific cell surface receptor molecule (CD4+) found on tissue dendritic cells, macrophages, and CD4+ T lymphocytes. The pathogenesis of infection, and the subsequent perpetuation of the disease state, involves a com- plex set of interactions by which HIV is able to take advantage of cellular pathways while avoiding or neutralizing various components of the immune system [11; 12]. The most common mode of HIV infection is sexual transmis- sion across exposed mucosal epithelium. Dendritic cells and macrophages are found beneath the mucosal epithelium of the anogenital and cervicovaginal tracts, as well as within tonsillar and adenoidal tissue. Studies in primates demonstrate that after the virus penetrates the mucosal epithelium, infection is initiated within nearby dendritic cells and macrophages.
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MDCT2026
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