Increasing rates of malarial fever with deteriorating immune status in HIV-1-infected Ugandan adults

French, Neil; Nakiyingi, Jessica; Lugada, Eric; Watera, Christine; Whitworth, James; Gilks, Charles F.

doi:10.1097/00002030-200105040-00010

Cited by 205 publications

(164 citation statements)

References 20 publications

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“…Make RPMI-0 by mixing 950 ml of ddH 2 O, 1 packet of RPMI-1640 powder, 6 g of HEPES, 2 g of sodium bicarbonate, and 1.35 mg of hypoxanthine. 2.…”

Section: Making Rpmi-a For Malaria Parasite Culturementioning

confidence: 99%

“…Areas of malaria and HIV endemicity share a wide geographic overlap, putting millions of people at risk of co-infection and consequently at risk for more severe clinical disease [2][3][4][5][6][7][8][9][10] . The two diseases negatively interact.…”

Section: Introductionmentioning

confidence: 99%

“…The two diseases negatively interact. In HIV-infected individuals, higher HIV viral loads and temporary decreases in CD4 + T-cell counts can be seen during a malaria infection, while malaria parasite burdens and risk of clinical and severe malaria are higher in co-infected individuals 2,3,5,7,8,10 . The mechanisms by which HIV increases malaria severity are not fully understood and warrant further investigation.…”

Section: Introductionmentioning

confidence: 99%

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An In Vitro Model for Measuring Immune Responses to Malaria in the Context of HIV Co-infection

Finney

Serghides

2015

JoVE

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Malaria and HIV co-infection is a growing health priority. However, most research on malaria or HIV currently focuses on each infection individually. Although understanding the disease dynamics for each of these pathogens independently is vital, it is also important that the interactions between these pathogens are investigated and understood.We have developed a versatile in vitro model of HIV-malaria co-infection to study host immune responses to malaria in the context of HIV infection. Our model allows the study of secreted factors in cellular supernatants, cell surface and intracellular protein markers, as well as RNA expression levels. The experimental design and methods used limit variability and promote data reliability and reproducibility.All pathogens used in this model are natural human pathogens (Plasmodium falciparum and HIV-1), and all infected cells are naturally infected and used fresh. We use human erythrocytes parasitized with P. falciparum and maintained in continuous in vitro culture. We obtain freshly isolated peripheral blood mononuclear cells from chronically HIV-infected volunteers. Every condition used has an appropriate control (P. falciparum parasitized vs. normal erythrocytes), and every HIV-infected donor has an HIV uninfected control, from which cells are harvested on the same day. This model provides a realistic environment to study the interactions between malaria parasites and human immune cells in the context of HIV infection. Video LinkThe video component of this article can be found at

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“…Make RPMI-0 by mixing 950 ml of ddH 2 O, 1 packet of RPMI-1640 powder, 6 g of HEPES, 2 g of sodium bicarbonate, and 1.35 mg of hypoxanthine. 2.…”

Section: Making Rpmi-a For Malaria Parasite Culturementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

An In Vitro Model for Measuring Immune Responses to Malaria in the Context of HIV Co-infection

Finney

Serghides

2015

JoVE

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“…However, others have shown that P. falciparum antigens induced HIV-1 replication in vitro (8) and in vivo (9). HIV-1 infection was also found to reduce the immunity of pregnant women (10,11) and increase the onset of malaria fever (12) in falciparum malaria cases.…”

Section: Introductionmentioning

confidence: 99%

Parasito-haematological features of acute Plasmodium falciparum and P. vivax malaria patients with and without HIV co-infection at Wonji Sugar Estate, Ethiopia

Kassa¹,

Petros

Messele³

et al. 2005

Ethiopian Journal of Health Development

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Background: Investigation to identify factors that determine the clinical outcome of malaria are essential for the improvement of patient care in severe malaria cases. Objectives: To assess the parasitologic and haemato-immunological characteristics of malaria patients with and without HIV co-infection. Methods: Immune cells were enumerated using the Flow cytometer method. Haematological values were determined using the Coulter Counter system. Malaria parasite detection was conducted using standard microscopy; and HIV testing was conducted using Determine, ELISA and Western blot methods. Results: A total of 253 study participants, out of which 87 were control cases, and 166 were acute malaria patients (49.4% due to P. falciparum, 48.8 % due to P. vivax, 1.8% due to mixed infection) were included. Eight out of 166 (4

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“…In Uganda, the prevalence of HIV is estimated to be 6.4% in adults and 0.7% in children, 1 The transmission intensity of malaria in Tororo, Uganda, the site of the study, is very high, with a parasite prevalence of 91% among children 2-9 years of age 2 and an entomologic inoculation rate of 562 infectious bites per person per year. 3 Past evidence has demonstrated that clinical malaria is more likely to develop in HIV-infected patients than in those who are uninfected, [4][5][6] with an estimated 10% of clinical malaria in Africa attributable to concurrent HIV infection. 7 Furthermore, HIV-infected women are at greater risk of acquiring placental malaria during pregnancy than HIV-uninfected women.…”

Section: Introductionmentioning

confidence: 99%

Plasmodium falciparum Dihydrofolate Reductase and Dihyropteroate Synthase Mutations and the Use of Trimethoprim-Sulfamethoxazole Prophylaxis among Persons Infected with Human Immunodeficiency Virus

Malamba

Sandison²,

Lule³

et al. 2010

The American Journal of Tropical Medicine and Hygiene

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Abstract. A prospective cohort design was used to measure the association between daily cotrimoxazole-prophylaxis and infection with Plasmodium falciparum containing mutations associated with antifolate resistance among persons infected with human immunodeficiency virus (HIV) in Tororo and Busia District, in eastern Uganda. Of 149 cases of P. falciparum parasitemia diagnosed, 147 (99%) (smears from participants taking prophylaxis = 91 and smears from those not taking cotrimoxazole prophylaxis = 56) were successfully assessed for mutations in the dihydrofolate reductase ( dhfr ) and dihydropteroate synthase ( dhps ) mutations associated with antifolate resistance. Prevalences of the dhfr pure triple mutant (74% and 70%; P = 0.71), the dhps pure double mutant (95% and 88%; P = 0.21), and the dhfr/dhps pure quintuple mutant (73% and 64%; P = 0.36), were not significantly different between those taking and those not taking cotrimoxazole-prophylaxis, respectively. The overall prevalence of the pure quintuple mutant in this study was 69%, which is among the highest in Africa. Although resistance rates of P. falciparum to antifolate drugs are high, cotrimoxazole-prophylaxis in HIV-infected persons was not associated with a higher prevalence of mutations associated with antifolate resistance.

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Increasing rates of malarial fever with deteriorating immune status in HIV-1-infected Ugandan adults

Cited by 205 publications

References 20 publications

An <em>In Vitro</em> Model for Measuring Immune Responses to Malaria in the Context of HIV Co-infection

An <em>In Vitro</em> Model for Measuring Immune Responses to Malaria in the Context of HIV Co-infection

Parasito-haematological features of acute <i>Plasmodium falciparum</i> and <i>P. vivax</i> malaria patients with and without HIV co-infection at Wonji Sugar Estate, Ethiopia

Plasmodium falciparum Dihydrofolate Reductase and Dihyropteroate Synthase Mutations and the Use of Trimethoprim-Sulfamethoxazole Prophylaxis among Persons Infected with Human Immunodeficiency Virus

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