Increased circulation time of Plasmodium falciparum underlies persistent asymptomatic infection in the dry season.
СтатьяПоддержка NIH: внешняя программаResearch Support, N.I.H., IntramuralПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Andrade Carolina M, Fleckenstein Hannah, Thomson-Luque Richard, Doumbo Safiatou, Lima Nathalia F, Anderson Carrie, Hibbert Julia, Hopp Christine S, Tran Tuan M, Li Shanping, Niangaly Moussa, Cisse Hamidou, Doumtabe Didier, Skinner Jeff, Sturdevant Dan, Ricklefs Stacy, Virtaneva Kimmo, Asghar Muhammad, Homann Manijeh Vafa, Turner Louise, Martins Joana, Allman Erik L, N'Dri Marie-Esther, Winkler Volker, Llinás Manuel, Lavazec Catherine, Martens Craig, Färnert Anna, Kayentao Kassoum, Ongoiba Aissata, Lavstsen Thomas, Osório Nuno S, Otto Thomas D, Recker Mario, Traore Boubacar, Crompton Peter D, Portugal Silvia
Аннотация
The dry season is a major challenge for Plasmodium falciparum parasites in many malaria endemic regions, where water availability limits mosquito vectors to only part of the year. How P. falciparum bridges two transmission seasons months apart, without being cleared by the human host or compromising host survival, is poorly understood. Here we show that low levels of P. falciparum parasites persist in the blood of asymptomatic Malian individuals during the 5- to 6-month dry season, rarely causing symptoms and minimally affecting the host immune response. Parasites isolated during the dry season are transcriptionally distinct from those of individuals with febrile malaria in the transmission season, coinciding with longer circulation within each replicative cycle of parasitized erythrocytes without adhering to the vascular endothelium. Low parasite levels during the dry season are not due to impaired replication but rather to increased splenic clearance of longer-circulating infected erythrocytes, which likely maintain parasitemias below clinical and immunological radar. We propose that P. falciparum virulence in areas of seasonal malaria transmission is regulated so that the parasite decreases its endothelial binding capacity, allowing increased splenic clearance and enabling several months of subclinical parasite persistence.