Complement effects on the infectivity of Plasmodium gallinaceum to Aedes aegypti mosquitoes. I. Resistance of zygotes to the alternative pathway of complement. (original) (raw)
Journal Article
Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health
,
Building 5, Room 112, Bethesda, MD 20892
Present address: Cynthia A. Grotendorst, Medical University of South Carolina, 171 Ashley Ave., Charleston, SC 29425.
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R Carter ,
Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health
,
Building 5, Room 112, Bethesda, MD 20892
Address all correspondence to: Dr. Richard Carter, Building 5, Room 112, NIH, NIAID, Bethesda, MD 20892.
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Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health
,
Building 5, Room 112, Bethesda, MD 20892
Present address: Dr. Ronald Rosenberg, Armed Forces Research Institute of Medical Sciences, Rajvithi Road, Bangkok, Thailand.
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Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health
,
Building 5, Room 112, Bethesda, MD 20892
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Received:
13 December 1985
Accepted:
20 February 1986
Cite
C A Grotendorst, R Carter, R Rosenberg, L C Koontz, Complement effects on the infectivity of Plasmodium gallinaceum to Aedes aegypti mosquitoes. I. Resistance of zygotes to the alternative pathway of complement., The Journal of Immunology, Volume 136, Issue 11, June 1986, Pages 4270–4274, https://doi.org/10.4049/jimmunol.136.11.4270
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Abstract
Gametocytes are the intraerythrocytic stages of malaria parasites that infect mosquitoes. When gametocytes of the chicken malaria parasite Plasmodium gallinaceum are ingested by a mosquito they become extracellular in the mosquito midgut, form gametes, and fertilize within 10 to 15 min after the insect has taken a blood meal. Gametocytes of P. gallinaceum were infectious when fed to Aedes aegypti mosquitoes in blood meals containing native serum from chickens or from the non-host species, man or sheep. Gametocytes stimulated to undergo gametogenesis and to fertilize in vitro were also infectious when fed to mosquitoes in native chicken serum. However, native serum from most non-host species, including sheep and man, suppressed the infectivity of newly fertilized zygotes to mosquitoes and lysed the zygotes in vitro. These effects were shown to be due to the activity of the alternative pathway of complement (APC) in the serum of the non-host species. After mild trypsin treatment, the zygotes of P. gallinaceum no longer infected mosquitoes in the presence of native chicken serum, although in heat-inactivated chicken serum their infectivity was normal. We conclude that trypsin-sensitive components on the zygotes surface protect them from destruction by the APC of their native host. The ability of gametocytes of P. gallinaceum to infect mosquitoes in the presence of native human serum is probably due to proteases that inactivate the APC of human serum before the gametes and zygotes emerge as extracellular parasites in the blood meal.
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Copyright © 1986 by American Association of Immunologists
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