Showing papers by "Jefferson A. Vaughan published in 1996"
TL;DR: These studies confirm an earlier report that malaria sporozoites can disrupt salivary gland barriers and enhance mosquito transmission of arboviruses and taken together with similar studies using microfilarial parasites, it is increasingly apparent that mosquito-borne parasites have the potential to enhance mosquito Transmission of Arbovirus.
Abstract: Certain mosquito species are susceptible to viral infection but cannot transmit the virus due to a salivary gland barrier. We hypothesized that such species could transmit virus if the mosquito were infected with both virus and malaria parasites. Malaria sporozoites disrupt the integrity of mosquito salivary glands and, in so doing, may destroy salivary gland barriers to viral transmission. To examine this postulate, the model system of Rift Valley fever (RVF) virus and a rodent parasite, Plasmodium berghei, in Anopheles stephensi mosquitoes was used. Viral transmission rates for RVF virus-inoculated anophelines that were previously fed either gametocytemic blood (malaria-infected) or normal blood (control) were compared. Viral transmission rates for anophelines having concurrent sporozoite infection of the salivary glands were 32% (n = 25). None of the RVF virus-inoculated control anophelines (n = 55) transmitted virus. These studies confirm an earlier report that malaria sporozoites can disrupt salivary gland barriers and enhance mosquito transmission of arboviruses. Taken together with similar studies using microfilarial parasites, it is increasingly apparent that mosquito-borne parasites have the potential to enhance mosquito transmission of arboviruses.
31 citations
TL;DR: It is suggested that certain key parameters determine whether dual virus/mf host infections will enhance arboviral infectivity to mosquitoes, including species differences in the capacity of mf to penetrate the mosquito midgut, the amount of virus passing into the hemocoel during mf penetration, and the innate susceptibility of mosquitoes to hemocoelsomically introduced virus.
Abstract: When mosquitoes feed on a vertebrate host that is infected concurrently with virus and microfilariae (mf), both pathogens are ingested. If mf penetrate the mosquito midgut, a small portion of the ingested virus may disseminate directly into the mosquito hemocoel. This phenomenon, termed microfilarial enhancement of arboviral transmission, has the potential to enhance the infectivity of arboviruses to mosquitoes. We investigated whether concurrent ingestion of Brugia mf and eastern equine encephalitis virus would enhance the infectivity and subsequent transmissibility of the virus by Aedes mosquitoes. Trials with Ae. triseriatus and B. pahangi mf indicated that microfilarial enhancement was dose dependent. Both a sufficient number of penetrating mf and a sufficient viremia were required for enhancement to occur. Furthermore, studies with B. malayi and three species of Aedes indicated that under comparable conditions of host viremia and microfilaremia, microfilarial enhancement occurred in some mosquito species (i.e., Ae. aegypti and Ae. taeniorhynchus) but not in others (Ae. triseriatus). We suggest that certain key parameters determine whether dual virus/mf host infections will enhance arboviral infectivity to mosquitoes. These include species differences in the capacity of mf to penetrate the mosquito midgut, the amount of virus passing into the hemocoel during mf penetration, and the innate susceptibility of mosquitoes to hemocoelomically introduced virus.
27 citations
TL;DR: The results show that fleas have calreticulin and, possibly, several isoforms, and it appears that the salivary glands of the cat and oriental rat flea differ in detectable levels of cal reticulin.
Abstract: Calreticulin has been defined in the cat flea, Ctenophalides felis (Bouche), and oriental rat flea, Xenopsylla cheopis (Rothschild). Calreticulin, a major endoplasmic reticulum protein, was previously identified as a component of ixodid tick saliva. Using a riboprobe generated from the tick calreticulin complementary DNA (cDNA), we distinguished 2 transcripts for calreticulin in cat fleas by Northern blot analysis. Increased expression of calreticulin was not evident in fed versus unfed adult fleas. We were able to amplify a calreticulin flea product from fed female messenger RNA (mRNA) using primers designed from the tick calreticulin gene. One of these products hybridized to the tick riboprobe. Localization of specific antibody to cat flea tissues showed calreticulin in the midgut with no detection in the salivary glands. We also observed specific labeling of calreticulin with antibody in the ovaries of fed females. Several cat flea polypeptides appear to crossreact with anticalreticulin antibody in Western blots. We did not detect a calreticulin using antibody to the tick-secreted protein in cat flea salivary glands. This antibody did recognize a protein in the rat flea salivary glands. Our results show that fleas have calreticulin and, possibly, several isoforms. It appears that the salivary glands of the cat and oriental rat flea differ in detectable levels of calreticulin. The specific antibody labeling of the ovaries is interesting and remains to be understood. Calreticulin's appearance in the midgut suggests a possible source of calreticulin as a flea secretion. Further studies are in progress to complete the sequencing of the flea polymerase chain reaction (PCR) product to compare to tick-secreted calreticulin. Comparisons to other blood-feeding arthropods at the protein and gene level are also being done. We hope to define further the expression of calreticulin in fleas, and in general, blood-feeding arthropods, with respect to its role in feeding and pathogen transmission.
27 citations