scholarly journals The Rare, the Best: Spread of Antimalarial-Resistant Plasmodium falciparum Parasites by Anopheles Mosquito Vectors

Author(s):  
Antoine Berry ◽  
Sandie Menard ◽  
Sandrine E. Nsango ◽  
Luc Abate ◽  
Didier Concordet ◽  
...  

Drug selection pressure in malaria patients is the cause of the emergence of resistant parasites. Resistance imposes a fitness cost for parasites in untreated infections, so withdrawal of the drug leads to the return of susceptible parasites.

mBio ◽  
2018 ◽  
Vol 9 (6) ◽  
Author(s):  
Johanna Patricia Daily

ABSTRACT The most advanced vaccine against Plasmodium falciparum malaria, RTS,S/AS01, provides partial protection in infants and children living in areas of malaria endemicity. Further understanding its mechanisms of protection may allow the development of improved second-generation vaccines. The RTS,S/AS01 vaccine targets the sporozoites injected by mosquito vectors into the dermis which then travel into the blood stream to establish infection in the liver. Flores-Garcia et al. (Y. Flores-Garcia, G. Nasir, C. S. Hopp, C. Munoz, et al., mBio 9:e02194-18, 2018, https://doi.org/10.1128/mBio.02194-18) shed light on early protective responses occurring in the dermis in immunized animals. They demonstrated that immunization impairs sporozoite motility and entry into blood vessels. Furthermore, they established that challenge experiments performed using a dermal route conferred greater protection than intravenous challenge in immunized mice. Thus, the dermal challenge approach captures the additional protective mechanisms occurring in the dermis that reflect the natural physiology of infection. Those studies highlighted the fascinating biology of skin-stage sporozoites and provided additional insights into vaccine-induced protection.


2016 ◽  
Vol 116 (2) ◽  
pp. 495-502 ◽  
Author(s):  
Kadarkarai Murugan ◽  
Jiang Wei ◽  
Mohamad Saleh Alsalhi ◽  
Marcello Nicoletti ◽  
Manickam Paulpandi ◽  
...  

2002 ◽  
Vol 32 (12) ◽  
pp. 1469-1476 ◽  
Author(s):  
A.M Nzila ◽  
E.K Mberu ◽  
E Nduati ◽  
A Ross ◽  
W.M Watkins ◽  
...  

2019 ◽  
Vol 10 ◽  
Author(s):  
Cheryl A. Kivisi ◽  
Michelle Muthui ◽  
Martin Hunt ◽  
Greg Fegan ◽  
Thomas Dan Otto ◽  
...  

Parasitology ◽  
1975 ◽  
Vol 71 (1) ◽  
pp. 41-49 ◽  
Author(s):  
H. D. Chapman

The development of drug resistance by the present Houghton strain of Eimeria tenella to the quinolones, methyl benzoquate and buquinolate, was found to take place after a single experimental passage. The development of resistance was independent of drug selection pressure and showed cross resistance to other quinolones, but not to amprolium and robenidine. When the Weybridge, Beltsville and Elberfeld strains of E. tenella were compared under similar laboratory conditions, the Weybridge and Elberfeld strains developed resistance to methyl benzoquate after 6 passages and the Beltsville after 5. Studies on the response of the Houghton strain to methyl benzoquate and buquinolate revealed that the drugs did not completely control the infection as measured by weight gain and that oocyst production was not suppressed. These observations indicate that the strain had already acquired some resistance to these drugs. This was confirmed by examining the resistance to methyl benzoquate of a culture of the Houghton strain of E. tenella which had been stored frozen in liquid nitrogen since 1969. This showed full sensitivity to the drug and developed resistance after 8 passages. This suggests that drug tolerance has been acquired by the Houghton strain since 1969.Oocyst lines were established from the Houghton strain by infecting single birds with approximately 10 oocysts. Eleven of these lines were found to be sensitive to methyl benzoquate, and nine to give rise to resistant parasites. It is concluded that the Houghton strain is contaminated by a small number of resistant oocysts which can be eliminated from a culture by dilution of the challenge inoculum. One of these Houghton oocyst lines, sensitive to methyl benzoquate, developed resistance after 8 serial passages.


2008 ◽  
Vol 41 (5) ◽  
pp. 1151-1158 ◽  
Author(s):  
Frank Baumgartner ◽  
Sabine Wiek ◽  
Kerstin Paprotka ◽  
Stefan Zauner ◽  
Klaus Lingelbach

RSC Advances ◽  
2015 ◽  
Vol 5 (59) ◽  
pp. 47959-47974 ◽  
Author(s):  
Rashmi Gaur ◽  
Harveer Singh Cheema ◽  
Yogesh Kumar ◽  
Suriya Pratap Singh ◽  
Dharmendra K. Yadav ◽  
...  

Cerebral malaria is a serious and sometimes fatal disease caused by aPlasmodium falciparumparasite that infects a female anopheles mosquito which feeds on humans.


2008 ◽  
Vol 52 (11) ◽  
pp. 4089-4097 ◽  
Author(s):  
Andrea M. McCollum ◽  
Leonardo K. Basco ◽  
Rachida Tahar ◽  
Venkatachalam Udhayakumar ◽  
Ananias A. Escalante

ABSTRACT Sulfadoxine-pyrimethamine (SP) resistance in Plasmodium falciparum is encoded by a number of mutations in the dihydrofolate reductase (dhfr) and dihydropteroate synthetase (dhps) genes. Here, we have characterized point mutations in dhfr and dhps and microsatellite loci around dhfr on chromosome 4 and dhps on chromosome 8 as well as neutral markers on chromosomes 2 and 3 in 332 samples from Yaoundé, Cameroon. The triple mutant dhfr haplotype that originated in Southeast Asia is the most predominant in this sample set, but we also find additional independent haplotypes at low frequency and an incipient process of genetic differentiation among alleles of Southeast Asian origin. As reported for other African populations, we find evidence of a selective sweep for resistant dhfr mutants in this Cameroonian population due to drug selection. Although we find evidence for a selective sweep in dhps mutants associated with SP resistance, the dynamics of dhps mutants appear different than those observed for dhfr mutants. Overall, our results yield support for the use of microsatellite markers to track resistant parasites; however, the detection of resistant dhfr alleles in low frequency, the evidence of divergence among dhfr alleles that share a common evolutionary origin, and the distinct dynamics of resistant dhps alleles emphasize the importance of comprehensive, population-based investigations to evaluate the effects of drug selection on parasite populations.


2012 ◽  
Vol 86 (2) ◽  
pp. 211-213 ◽  
Author(s):  
Grace O. Gbotosho ◽  
Onikepe A. Folarin ◽  
Carolina Bustamante ◽  
Ayoade M. J. Oduola ◽  
Christian T. Happi ◽  
...  

1998 ◽  
Vol 72 (5) ◽  
pp. 3773-3778 ◽  
Author(s):  
P. Richard Harrigan ◽  
Stuart Bloor ◽  
Brendan A. Larder

ABSTRACT Replication of mixtures of two or more human immunodeficiency virus type 1 (HIV-1) variants would be expected to result in the eventual selection of the fittest virus due to Darwinian competition among the variants. The relative proportions of known HIV-1 variants (which may differ only by a single nucleotide from a standard “wild-type” virus, HIV-1HXB2) in mixed viral cultures were quantified by analysis of automated sequence signals of reverse transcriptase PCR products. With this method, the relative levels of replicative fitness of several zidovudine (3′-azidothymidine)-resistant HIV-1HXB2 variants were estimated under controlled in vitro conditions by measuring the rate of change in the proportions of viral variants as they replicated in cell cultures both in the presence and in the absence of drug selection pressure. These variants were engineered to contain commonly observed zidovudine resistance mutations in the HIV-1 reverse transcriptase (M41L, K70R, T215Y, and M41L+T215Y). In the absence of zidovudine, all variants tested displayed reduced replicative fitness compared to wild-type HIV-1HXB2. The order of relative fitness was wild type > K70R ≫ T215Y = M41L+T215Y > M41L. Mixed cultures in the presence of zidovudine showed a dose-dependent selection pressure against the wild-type virus which varied according to the resistance profile of each virus. The information gathered from this approach provides insight into competition among multiple HIV-1 variants, which likely occurs in vivo with drug selection pressure, and may be applicable in more complex mathematical models for predicting the emergence of HIV-1 variants after the initiation of antiretroviral therapy.


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