Last reviewed: November 2017
Last updated: November  2017


Conditions relevant to HIV (Overview)


HIV replicates primarily in CD4 cells and macrophages, and can be transmitted via blood, blood products, sexual fluids, other fluids containing blood, and breast milk. The CD4 cell count indicates the health of the immune system. An average CD4 count for an HIV-negative adult is 800 cells/microlitre. People with a CD4 count >500 cells/microlitre are usually asymptomatic. A CD4 count <350 cells/microlitre implies substantial immune suppression, and a CD4 count <200 cells/microlitre places patients at risk of most opportunistic infections. Pneumocystis jirovecii pneumonia is the most common initial opportunistic infection. The decision to initiate highly active antiretroviral therapy (HAART) to treat HIV depends on the patient's clinical stage, CD4 count, medical comorbidities, and ability to adhere to chronic HIV treatment. Early treatment may be beneficial in all patients.

Perinatal transmission is the most common route of HIV infection in children. When HIV is diagnosed before or during pregnancy, perinatal transmission can be reduced to <1% with preventive measures. Since the mid-1990s, HIV testing and preventive interventions have resulted in >90% reduction in perinatal HIV infections in the US. [4] To prevent vertical transmission, highly active antiretroviral therapy (HAART) is initiated as soon as possible in the pregnancy irrespective of CD4 count or viral load.

HIV-related opportunistic infections (OIs) are clinical syndromes that arise as a consequence of impaired immunity in advanced stages of HIV infection. These illnesses tend to occur most often in patients who have untreated HIV infection or who fail to benefit from antiretroviral therapy. Tuberculosis, Pneumocystis jirovecii pneumonia (PCP), candidiasis, cryptococcosis, toxoplasmosis, CMV, mycobacterium avium complex (MAC) infections, Herpes simplex virus infection (HSV), and cryptosporidiosis are among the HIV-related OIs often encountered in clinical practice. [5]

Formerly known as Pneumocystis carinii , it is one of the most common AIDS-defining illnesses in resource-rich countries. Suspicion for PCP is based on clinical signs or symptoms of pneumonia in a person with immune suppression, especially when due to HIV infection. Diagnosis is made by detection of the organism in either induced sputum or bronchoalveolar lavage (BAL) or, less commonly, in lung tissue.

Infection with Mycobacterium tuberculosis (MTB) is transmitted by inhalation of particles containing tubercle bacilli. [6] HIV infection is an independent risk factor for acquisition of TB and rapid progression to disease. Defects of cellular immunity and macrophage function have been demonstrated in HIV-infected people with TB. [7] TB can be overlooked as it may present with signs and symptoms (e.g., fevers, weight loss, malaise) mistakenly attributed to HIV itself. Depending on the involved site, TB may present with shortness of breath, cough, lymphadenopathy, headache, meningism, abdominal pain, dysuria, or abscess formation. The clinical manifestations of pulmonary TB may be different depending on the level of immunosuppression in HIV-infected people [8] and a high index of suspicion must be maintained when evaluating an HIV-infected patient with symptoms suggestive of TB, as chest x-rays may appear normal in some patients, such as those with advanced HIV. [9]

Also known as mycobacterium avium complex (MAC), mycobacterium avium-intracellulare (MAI) consists of 2 mycobacterium species, M avium and M intracellulare , [10] which are commonly found in the environment (soil, water, and animals). [11] Colonisation of the intestinal tract with MAI is believed to be the primary route of MAI infection in patients with AIDS, and precedes the appearance of bacteraemia and disseminated disease by several months. [12] [13] Prior to the availability of highly active antiretroviral therapy (HAART), disseminated MAI occurred in 20% to 40% of AIDS patients. [14] HIV-infected patients with a CD4 cell count <50 cells/microlitre are at increased risk of infection. Presenting features include non-specific symptoms and signs or worsening of chronic constitutional symptoms (e.g., persistent fever, night sweats, fatigue, weight loss, and anorexia).

A low-grade vasoformative neoplasm associated with human herpesvirus-8 (HHV-8) or Kaposi's sarcoma herpesvirus (KSHV) infection. [15] It is the most common neoplasm arising in HIV-positive individuals. Lesions frequently involve mucocutaneous sites, but may become more extensive to involve the lymph nodes and visceral organs. Skin lesions evolve from an early patch, to a plaque, and later to ulcerating tumour nodules. In HIV-positive people, highly active antiretroviral therapy (HAART) without treatment interruptions may help prevent Kaposi's sarcoma (KS) or result in a less-aggressive presentation. AIDS patients with KS should adhere to an effective, uninterrupted antiretroviral regimen in order to avoid disease progression and/or the development of new KS lesions. Non-nucleoside reverse transcriptase inhibitor (NNRTI)-based regimens are as effective as protease inhibitor (PI)-based regimens in terms of protection. [16]

This infection is caused by Toxoplasma gondii and can be transmitted either through ingestion of oocysts from undercooked meat, other food or water contaminated with oocysts, by transplacental spread of tachyzoites, or through direct contact with cat faeces. Acute infection is usually asymptomatic and, once acquired, parasites remain in human tissues for the duration of their lifespan. Symptomatic disease can be seen in immunocompromised patients with reactivation of latent infection or with acquisition of new infection. Symptomatic eye disease can be seen in both immunocompromised and immunocompetent patients. In HIV-infected patients, most toxoplasmosis cases arise from reactivation of latent infection from a remote exposure. [17] [18]

Cryptococcus neoformans is an encapsulated free-living fungus that can be isolated from soils and avian excreta. Infection may occur through inhalation of aerosolised organisms from environmental sources. Increased exposure to environmental sources of the organism or increased susceptibility due to impaired immunity predispose HIV-infected people to cryptococcosis. [19] [20] In immunocompromised patients, cryptococcosis usually presents as a subacute meningitis or meningoencephalitis with fever, malaise, and headache. However, disseminated disease can occur, with or without concurrent meningitis. In such cases, pulmonary involvement or skin lesions may be present.

Cytomegalovirus (CMV) is a member of the herpesvirus family. It thus remains latent in the infected host following primary infection and can be transmitted via person to person (intimate contact), vertical transmission (mother to child, resulting in congenital infection), blood transfusion, and organ or haematopoietic stem cell transplantation. [21] In patients with AIDS, progressive loss of cell-mediated immunity permits CMV reactivation and replication to begin and results in tissue necrosis in association with non-specific inflammation. [22] Retinitis is the most common clinical presentation in people with AIDS and CMV disease. Other manifestations include colitis (second most common), cholangitis, encephalitis, [23] pneumonitis, and gastritis. Pain and weakness may indicate the presence of CMV polyradiculopathy. [24]

This is a fungal infection of the mucosa caused in most cases by Candida albicans , and occasionally by C glabrata , C tropicalis , C parapsilosis , C guilliermondii , C dubliniesis , and C krusei . [25] [26] [27] [28] An impairment in the host defence mechanisms and higher levels of plasma HIV RNA have been associated with increased rates of mucocutaneous candidiasis and colonisation with Candida. [29] [30] [31] Patients may present with oral (pseudomembranous candidiasis), oesophageal, or vaginal infection. Manifestations include altered taste sensation and/or pain or difficulty with swallowing in oral thrush or oesophageal disease; and erythema, itching, watery to curd-like vaginal discharge, dyspareunia, and swelling of the labia and vulva with discrete pustulopapular peripheral lesions in vaginal disease.

Post-exposure prophylaxis (PEP) is the administration of highly active antiretroviral therapy (HAART) to HIV-negative people who have been occupationally or sexually exposed to HIV. Once exposed to HIV, there may be a brief period before the infection is established, during which HAART may successfully prevent viral replication. [32] [33] PEP should optimally be given within a 72-hour window from exposure, and a 28-day course of treatment is recommended. [34]

Causes of altered mental status in HIV infection include both acutely presenting conditions (which often represent HIV-related opportunistic infection or associated systemic illness) and more progressive neurocognitive disease or psychological comorbidity. Neuropsychological issues arise as a direct effect of HIV infection: for example, as part of a spectrum of HIV-associated neurocognitive disorders (HAND) or as a psychiatric comorbidity (e.g., depression or alcohol/substance abuse).

Cutaneous manifestations often reflect immune status and may offer insight into the long-term prognosis of HIV-infected patients. The aetiologies of different diseases involving the entire spectrum of skin and HIV vary, but a useful aetiological distinction to note is that some skin diseases are fairly specific to HIV (e.g., Kaposi's sarcoma, oral hairy leukoplakia, papular pruritic eruption of HIV, HIV photodermatitis), and other skin diseases may appear in non-HIV-infected populations but have altered presentation with HIV. The aetiology may be infectious, inflammatory, neoplastic, metabolic, or drug-related.



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