Effect of malaria on HIV-1 progression and transmission

Whitworth, James; Hewitt, Kirsten

doi:10.1016/s0140-6736(05)17752-6

Cited by 35 publications

(22 citation statements)

References 13 publications

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“…These findings agree with the current view that parasite immunity may require ageing to develop, but subsequently can persist without high antibody titres and therefore be maintained by occasional infrequent boosting [7][8][9]. Peaks in parasitaemia above 30 y of age present across endemic levels in eastern Tanzania might reflect malaria-HIV co-infection [31] and are not expected to be captured by the model. Incorporating a prolonged duration of (subpatent) infections, i.e., continual reinfection that prolongs infection and boosts an immune response that allows parasitaemia to persist at subpatent levels, worsened the model predictions.…”

Section: Discussionsupporting

confidence: 85%

Determination of the processes driving the acquisition of immunity to malaria using a mathematical transmission model

Filipe¹,

Riley²,

Drakeley³

et al. 2005

PLoS Comput Biol

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Acquisition of partially protective immunity is a dominant feature of the epidemiology of malaria among exposed individuals. The processes that determine the acquisition of immunity to clinical disease and to asymptomatic carriage of malaria parasites are poorly understood, in part because of a lack of validated immunological markers of protection. Using mathematical models, we seek to better understand the processes that determine observed epidemiological patterns. We have developed an age-structured mathematical model of malaria transmission in which acquired immunity can act in three ways (''immunity functions''): reducing the probability of clinical disease, speeding the clearance of parasites, and increasing tolerance to subpatent infections. Each immunity function was allowed to vary in efficacy depending on both age and malaria transmission intensity. The results were compared to age patterns of parasite prevalence and clinical disease in endemic settings in northeastern Tanzania and The Gambia. Two types of immune function were required to reproduce the epidemiological age-prevalence curves seen in the empirical data; a form of clinical immunity that reduces susceptibility to clinical disease and develops with age and exposure (with half-life of the order of five years or more) and a form of anti-parasite immunity which results in more rapid clearance of parasitaemia, is acquired later in life and is longer lasting (half-life of .20 y). The development of anti-parasite immunity better reproduced observed epidemiological patterns if it was dominated by age-dependent physiological processes rather than by the magnitude of exposure (provided some exposure occurs). Tolerance to subpatent infections was not required to explain the empirical data. The model comprising immunity to clinical disease which develops early in life and is exposure-dependent, and anti-parasite immunity which develops later in life and is not dependent on the magnitude of exposure, appears to best reproduce the pattern of parasite prevalence and clinical disease by age in different malaria transmission settings. Understanding the effector mechanisms underlying these two immune functions will assist in the design of transmission-reducing interventions against malaria.

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Section: Discussionsupporting

confidence: 85%

Determination of the processes driving the acquisition of immunity to malaria using a mathematical transmission model

Filipe¹,

Riley²,

Drakeley³

et al. 2005

PLoS Comput Biol

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“…This is confirmed by research findings which indicate that in sub-Saharan Africa, with an HIV prevalence of 8%, adult malaria secondary to HIV is 4% parasitaemia and 5% clinical malaria. In southern Africa, where the HIV prevalence is 30%, these rates increase to 20% and 30% [18].…”

Section: Discussionmentioning

confidence: 99%

Assessment of the impact of malaria on CD4+ T Cells and haemoglobin levels of HIV-malaria co-infected patients

Tagoe

Boachie

2012

J Infect Dev Ctries

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Introduction: The human immunodeficiency virus (HIV) and malaria destroy important cells required for proper immunological and haematological functioning of the body. This research therefore aimed to assess the effect of malaria on CD4+ and haemoglobin (Hb) levels of HIV-malaria co-infected patients. Methodology: The study was performed by sampling 220 adult HIV patients on highly active anti retroviral therapy (HAART) who routinely visited the Tema General Hospital in Ghana. Blood samples were obtained for both blood film microscopy identification of malaria parasites and analysis using rapid diagnostic test kits. A BD Facscount Analyzer was used in the quantification of CD4+ levels. Results: Of the 220 patients sampled, 34 (15.5%) were HIV-malaria co-infected, all of whom (34; 100%) had CD4+ counts below the normal range, while 23 (12.9%) of the HIV mono-infected patients had normal CD4+ counts. Almost all HIV-malaria co-infected patients (33; 97.1%) had low Hb levels, whereas 79 (42.5%) of the HIV mono-infected patients had normal Hb. Malaria infection strongly correlated positively and significantly with both low CD4+ count (χ2 = 0.828, P = 0.003) and Hb (χ2 = 0.817, P = 0.004) levels. Conclusion: Malaria co-infection with HIV decreases CD4+ T cells and Hb levels in patients. It is therefore recommended that HIV patients in malaria endemic areas should adhere to malaria preventive measures.

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“…ITNs prevent malaria among children and pregnant women when distributed at a community-level (Lengeler, 2004;Ter Kuile, 2003a, 2003b, and among adults with HIV (Mermin, 2006a). The high incidence and potentially poor outcomes of malaria among people with HIV supports the use of ITNs in HIV-infected populations (Korenromp, 2005;Kublin, 2005;Mermin, 2006b;Whitworth, 2005).…”

Section: Discussionmentioning

confidence: 99%

Utilization of a basic care and prevention package by HIV-infected persons in Uganda

et al. 2008

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Opportunistic infections are the leading cause of mortality among HIV-infected people. Several simple interventions prevent illness, prolong life, or prevent HIV transmission from HIV-infected people in Africa. These include: cotrimoxazole prophylaxis; insecticide-treated bed nets; supplies for household water treatment and safe storage; materials promoting family voluntary counselling and testing (VCT); and condoms. We provided these interventions to adults and children with HIV who were members of the AIDS Support Organization in Uganda. To evaluate use of this basic care and prevention package, we surveyed a representative sample of 112 clients of TASO in their homes. Among respondents, 95% reported taking cotrimoxazole everyday, 89% said they had slept under a bednet the night before, 65% reported current treatment of household drinking water, 89% of sexually active respondents reported using condoms, and 96% reported family use of VCT. Household observations verified that use of cotrimoxazole, bednets, and water treatment products were consistent with reported use. This evaluation suggests successful distribution and use of basic care and prevention services at an AIDS organization in Uganda.

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Effect of malaria on HIV-1 progression and transmission

Cited by 35 publications

References 13 publications

Determination of the processes driving the acquisition of immunity to malaria using a mathematical transmission model

Determination of the processes driving the acquisition of immunity to malaria using a mathematical transmission model

Assessment of the impact of malaria on CD4+ T Cells and haemoglobin levels of HIV-malaria co-infected patients

Utilization of a basic care and prevention package by HIV-infected persons in Uganda

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