Malarial attacks are fuelling HIV transmission on a large scale, and prompt treatment of malaria could signficantly reduce sexual transmission of HIV, according to a major epidemiological modelling exercise published this month by the journal Science. The study also shows that where HIV prevalence is high and malaria incidence historically low, malaria incidence can grow alarmingly due to the reduced immunity in the population.
The Millenium Development Goals specifically targeted HIV/AIDS and malaria as major impediments of socio-economic development in Africa where an estimated 25.4 million people live with HIV/AIDS (PLWA) and over 3 million die annually. Malaria afflicts over 500 million people and kills about one million annually.
Malaria and HIV co-exist in most of Sub-saharan Africa. There has been an increasing litany of reports highlighting the impact of HIV/malaria coinfections on the course of each disease. The public health systems in Africa have been slow to adopt appropriate policies for the care of people with HIV in respect of malarial coinfection.
HIV destroys CD4 cells, the very immune cells which are critical for the development of antimalarial immunity. HIV-infected pregnant women show an increased incidence and severity of clinical malaria. In non-pregnant adults, HIV infection roughly doubles the risk of malaria parasitemia and clinical malaria. Anaemia is common and associated with increased mortality in HIV-infected children.
The efficacy of antimalarial treatment depends on the synergy between antimalarial drugs which clear drug-sensitive parasites and host immunity which clears drug-resistant parasites. Five studies in Ethiopia, Uganda, Kenya, Zambia, and Malawi have demonstrated that HIV/AIDS has a significant negative impact on the efficacy of antimalarial treatment. By contrast, there is a paucity of information on the impact of malaria on the efficacy or toxicity of antiretroviral drugs (ARV).
The mitochondrial toxicity of some ARV presents clinical manifestations which overlap with that of severe malaria caused by a direct effect of parasite sequestration or malaria-induced inflammatory cytokines on mitochondrial function. Malaria clinical attacks might therefore aggravate the ARV-mediated mitochondrial toxicity in PLWA. Some ARV might also exacerbate the metabolic disorder caused by severe malaria. More research is required on this aspect of HIV/malaria interaction as antiretrovirals become more accessible in Africa.
Malaria in HIV-positive people increases HIV viral loads and constitutes an important risk factor for HIV transmission to sexual partners and to unborn babies. It has not been feasible for logistical and ethical reasons to establish whether recurrent malaria promote HIV transmission in human populations and whether an escalating HIV/AIDS problem might push the current borders of malaria endemicity into those regions with unstable malaria transmission. A team of US investigators have addressed these issues using a mathematical model.
The core assumptions of the model included the rate of HIV transmission during sexual intercourse, increase in viral load during malaria attacks of various severity, HIV-mediated susceptibility to malaria as a function of the stage of HIV progression, duration of malaria-mediated viral load increments, sexual activity during clinical and non-clinical malaria, proportion of HIV-negative and HIV-positive people developing clinical malaria, and HIV mortality in dually infected patients in areas of stable and unstable malaria.
Malaria and HIV data from Kisumu, Kenya, an area of high HIV and malaria prevalence, was entered into the model. The impact of HIV/malaria interactions on each other’s prevalence in Kisumu and other settings with varying malaria and HIV prevalence was assessed.
In Kisumu, the interaction resulted in an HIV epidemic peak 8 % higher and a malaria peak 13 % higher than the levels in a scenario with no HIV/malaria interaction. The model shows that since 1990, Kisumu alone showed an excess of 8,500 HIV infections and 980,000 malaria attacks due to the interaction. In general, malaria accelerated the spread of HIV.
In scenarios where both malaria and HIV prevalence is high, the impact of the interaction was minimal. However, when one baseline prevalence was high while the other was low, co-infection increased HIV or malaria prevalence. For example, in a scenario with 1 % malaria and 37.8 % HIV prevalence, co-infection increased malaria prevalence about 9 fold (to 9.2 %) while it had minimal impact on HIV prevalence (38.5%).
Thus, areas with high endemicity for one disease but a low or unstable prevalence of the other are particularly at high risk for HIV/malaria interaction. In African settings such as southern Africa with unstable malaria transmission and an escalating HIV prevalence, HIV/malaria interaction might drive malaria transmission to stability.
The model was also used to assess the impact of anti-HIV and anti-malarial interventions. Malaria treatment was more effective in reducing malaria prevalence but it had no impact on HIV prevalence; shortening the persistence of the sexual stages of malaria to less than one month practically eliminated HIV-mediated malaria prevalence.
During malaria episodes, a 36 % reduction of sexual activity removed all excess HIV prevalence. Indeed, sexual abstinence during and for 4 weeks after a malaria attack would considerably reduce HIV prevalence. However, the authors point out that since the promotion of abstinence might not be feasible, early antimalarial treatment, providing anti-mosquito protective measures, and linking health services for malaria and HIV for PLWA would be the best control strategy.
In conclusion, transient but recurrent viral load surges in PLWA which are associated with repeated malaria attacks increase HIV prevalence and fuels the spread of each other on a population level. However, effective and prompt antimalarial malaria control, alongside abstinence and condom use, might effectively curtail the increase and spread of HIV.
The study by Abu-Raddad et al is a wake up call for public health authorities in Africa and development partners to take urgent and effective measures to confront this looming public health disaster in order to meet the Millenium Development Goals.
Abu-Raddad et al. Dual infection with HIV and malaria fuels the spread of both diseases in sub-Saharan Africa. Science 314: 1603-1606, 2006.