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HIV, like other retroviruses, depends on a unique enzyme, reverse transcriptase (RNA-dependent DNA polymerase), to replicate within host cells The other major pathogenic human retrovirus, human T cell lymphotropic/leukemia virus (HTLV)-I, is associated with lymphoma, while HIV is not known to be directly oncogenic The HIV genomes contain genes for three basic structural proteins and at least five other regulatory proteins; gag codes for group antigen proteins, pol codes for polymerase, and env codes for the external envelope protein The greatest variability in strains of HIV occurs in the viral envelope Since neutralizing activity is found in antibodies directed against the envelope, this variability presents problems for vaccine development In addition to the classic AIDS virus (HIV-1), a group of related viruses, HIV-2, has been isolated in West African patients HIV-2 has the same genetic organization as HIV-1, but there are significant differences in the envelope glycoproteins Some infected individuals exhibit AIDS-like illnesses, but most West Africans infected with HIV-2 are currently asymptomatic HIV-2 has been found in several people in the United States Thus, this variant may be less pathogenic or have a longer period of latency preceding disease Cases have been documented in which AIDS-like illnesses have occurred in the absence of HIV infection or other known infectious causes of immunodeficiency

Other cells in the immune network that are infected by HIV include B lymphocytes and macrophages The defect in B cells is partly due to disordered CD4 lymphocyte function These direct and indirect effects can lead to generalized hypergammaglobulinemia and can also depress B cell responses to new antigen challenges Because of these defects, the immunodeficiency of HIV is mixed Elements of humoral and cellular immunodeficiency are present, especially in children Macrophages act as a reservoir for HIV and serve to disseminate it to other organ systems (eg, the central nervous system) Apart from the immunologic effects of HIV, the virus can also directly cause a variety of neurologic effects Neuropathology largely results from the release of cytokines and other neurotoxins by infected macrophages Perturbations of excitatory neurotransmitters and calcium flux may contribute to neurologic dysfunction Direct HIV infection of renal tubular cells and gastrointestinal epithelium may contribute to these organ system manifestations of infection

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Clinically, the syndromes caused by HIV infection are usually explicable by one of three known mechanisms: immunodeficiency, autoimmunity, and allergic and hypersensitivity reactions

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Immunodeficiency is a direct result of the effects of HIV upon immune cells A spectrum of infections and neoplasms is seen, as in other congenital or acquired immunodeficiency states Two remarkable features of HIV immunodeficiency are the low incidence of certain infections such as listeriosis and aspergillosis and the frequent occurrence of certain neoplasms such as lymphoma or Kaposi s sarcoma This latter complication has been seen primarily in MSM or in bisexual men, and its incidence has steadily declined through the first 15 years of the epidemic A herpesvirus (KSHV or HHV-8) is the cause of Kaposi s sarcoma

Autoimmunity can occur as a result of disordered cellular immune function or B lymphocyte dysfunction Examples of both lymphocytic infiltration of organs (eg, lymphocytic interstitial pneumonitis) and autoantibody production (eg, immunologic thrombocytopenia) occur These phenomena may be the only clinically apparent disease or may coexist with obvious immunodeficiency Moreover, HIV-infected individuals appear to have higher rates of allergic reactions to unknown allergens as seen with eosinophilic pustular folliculitis ( itchy red bump syndrome ) as well as increased rates of hypersensitivity reactions to medications (for example, the fever and sunburn-like rash seen with trimethoprim-sulfamethoxazole reactions)

The hallmark of symptomatic HIV infection is immunodeficiency caused by continuing viral replication The virus can infect all cells expressing the T4 (CD4) antigen, which HIV uses to attach to the cell Chemokine receptors (CCR5 and CXCR4) are important for virus entry, and individuals with CCR5 deletions are less likely to become infected, and, once infected, the disease is more likely to progress slowly Once it enters a cell, HIV can replicate and cause cell fusion or death A latent state is also established, with integration of the HIV genome into the cell s genome The cell principally infected is the CD4 (helper-inducer) lymphocyte, which directs many other cells in the immune network With increasing duration of infection, the number of CD4 lymphocytes falls Some of the immunologic defects, however, are explained not by quantitative abnormalities of lymphocyte subsets but by qualitative defects in CD4 responsiveness induced by HIV

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The complications of HIV-related infections and neoplasms affect virtually every organ The general approach to the HIVinfected person with symptoms is to evaluate the organ

The find command searches the directory tree for all files that match the base filename specified by -name (in this case, all files ending in .c). The output of the find command is piped to wc, which counts the number of lines in each file (-l) and displays the totals. Here is the output for the find command and the entire command:

500 Absolute CD4 lymphocyte count (/mcL)

Bacterial infections Tuberculosis Herpes simplex Herpes zoster Vaginal candidiasis Hairy leukoplakia Kaposi's sarcoma

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