This review summarizes accumulating evidence of interactions between HIV and malaria and implications related to prevention and treatment of co-infection. HIV-infected persons are at increased risk for clinical malaria; the risk is greatest when immune suppression is advanced. Adults with advanced HIV may be at risk for failure of malaria treatment, especially with sulfa-based therapies. Malaria is associated with increases in HIV viral load that, while modest, may impact HIV progression or the risk of HIV transmission. Cotrimoxazole prophylaxis greatly reduces the risk of malaria in people with HIV; the risk can be further reduced with antiretroviral treatment and the use of insecticide treated mosquito nets. Increased numbers of doses of intermittent preventive treatment during pregnancy can reduce the risk of placental malaria in women with HIV. Interactions between malaria and HIV have important public health implications. People with HIV should use cotrimoxazole and insecticide treated mosquito nets. Malaria prevention is particularly important for pregnant women with HIV, although more information is needed about the best combination of strategies for prevention. In people with HIV, malaria diagnoses should be confirmed, highly effective drugs should be used for treatment, and possible drug interactions should be considered.

Serum copper concentration was measured in 80 adult patients (40 males and females each; age range: 18-40 yr) presenting with acute, uncomplicated falciparum malaria infection and a control group of 20 age-matched, healthy individuals. The mean serum copper concentration was 109.0 + 40.0 microg/dL in healthy individuals. Both male and female patients were found to have a significantly decreased serum copper concentration (p < 0.05). In the male patients, the mean serum copper concentration decreased by 33.95%, whereas it dropped by 38.53% in their female counterparts. A compromised enzymatic antioxidant defense capability, particularly superoxide dismutase (SOD) activity, has been reported in patients with falciparum malaria infection. Because SOD activity is dependent on copper, the ineffective SOD activity can be related to the decrease in the concentration of copper during the infection. Low serum copper can also contribute to the ineffective immune response of the host to the antigenic challenge of the falciparum parasite because copper is also important for normal immune function.