Feeding Virus Research Articles

Two Alimentary Canal Proteins, Fo-GN and Fo-Cyp1, Act in Western Flower Thrips, Frankliniella occidentalis TSWV Infection.

Tomato spotted wilt virus (TSWV) is a plant virus that causes massive economic damage to high-valued crops. This virus is transmitted by specific thrips, including the western flower thrips, Frankliniella occidentalis. TSWV is acquired by the young larvae during feeding on infected host plants. TSWV infects the gut epithelium through hypothetical receptor(s) and multiplies within the cells for subsequent horizontal transmission to other plant hosts via the salivary glands during feeding. Two alimentary canal proteins, glycoprotein (Fo-GN) and cyclophilin (Fo-Cyp1), are thought to be associated with the TSWV entry into the gut epithelium of F. occidentalis. Fo-GN possesses a chitin-binding domain, and its transcript was localized on the larval gut epithelium by fluorescence in situ hybridization (FISH) analysis. Phylogenetic analysis indicated that F. occidentalis encodes six cyclophilins, in which Fo-Cyp1 is closely related to a human cyclophilin A, an immune modulator. The Fo-Cyp1 transcript was also detected in the larval gut epithelium. Expression of these two genes was suppressed by feeding their cognate RNA interference (RNAi) to young larvae. The RNAi efficiencies were confirmed by the disappearance of the target gene transcripts from the gut epithelium by FISH analyses. The RNAi treatments directed to Fo-GN or Fo-Cyp1 prevented the typical TSWV titer increase after the virus feeding, compared to control RNAi treatment. Our immunofluorescence assay using a specific antibody to TSWV documented the reduction of TSWV in the larval gut and adult salivary gland after the RNAi treatments. These results support our hypothesis that the candidate proteins Fo-GN and Fo-Cyp1 act in TSWV entry and multiplication in F. occidentalis.

Pathogenesis of simian foamy virus infection in natural and experimental hosts

Inoculation of simian foamy virus type 1 into New Zealand white rabits resulted in an infection which was very similar to that observed in naturally infected nonhuman primates. Both intraperitoneal and intranasal inculations were found to be efficient procedures for the establishment of the infection in rabbits. Infection by the nasal route was found to be the best method, whereas no infection could be established by feeding virus in the drinking water. Once infection was established, virus persisted in the tissues and organs for as long as 264 days after inoculation, during which time the animals maintained significant levels of neutralizing antibody. Infectious virus was recovered from spleen, liver, lung, salivary gland, kidney, and, to a lesser extent, the brain. Virus was isolated from the blood only during early infection and never from the urine. A comparison of the distribution of foamy virus in naturally infected monkeys and baboon with experimentally infected rabbits showed that both groups harbored infectious virus in the same internal tissues and organs. Recovery of infectious virus from both groups of animals was accomplished by cultivation and/or co-cultivation of infected cells onto Vero cells.

Experimental infection of monkeys with Langat virus. 3. Infection produced by virus feeding.

Experimental infection of monkeys with Langat virus. 3. Infection produced by virus feeding.

Distribution of Coxsackie Virus in Experimentally Infected Cockroaches, Periplaneta americana.

SummaryGastrointestinal tracts removed at 5-day intervals for up to 20 days from cockroaches, Periplaneta americana, fed a single meal of Coxsackie virus contained sufficient virus to paralyze and kill test mice. Salivary glands removed after 5 days from the test cockroaches also caused paralysis and death in test mice; in one experiment, salivary glands removed 5, 10 and 20 days after a single feeding of virus caused Coxsackie infection in test mice.

IMMUNIZATION from paralytic poliomyelitis.

Editorial1 June 1953IMMUNIZATION FROM PARALYTIC POLIOMYELITISP. W. C.P. W. C.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-38-6-1339 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptInfantile paralysis strikes its victims in such a spectacular manner and is often so devastating that it arouses consternation and general sympathy. This has stimulated a huge volume of investigation which would be out of all proportion to the importance of the disease if this were judged solely by the frequency of its occurrence. The necessity until recently of utilizing monkeys exclusively in the experimental study of the disease has greatly restricted the scope of such investigations. However, the availability of liberal grants of funds for such studies and the recent introduction of new technical procedures have rapidly advanced our...1 EndersWellerRobbins JFTHFC: Cultivation of the Lansing strain of poliomyelitis virus in cultures of various human embryonic tissues, Science 109: 85, 1949. CrossrefMedlineGoogle Scholar2 Faber HK: Pathogenesis and onset of symptoms of poliomyelitis, Pediatrics 6: 488-497, 1950. MedlineGoogle Scholar3 Bodian D: A reconsideration of the pathogenesis of poliomyelitis, Am. J. Hyg. 55: 414-438, 1952. MedlineGoogle Scholar4 Horstman DM: Poliomyelitis virus in the blood of orally infected monkeys and chimpanzees, Federation Proc. 11: 471, 1952. Google Scholar5 Hammon WM: Immunity in poliomyelitis, Bacteriol. Rev. 13: 135-159, 1949. CrossrefMedlineGoogle Scholar6 Bodian D: Experimental studies on passive immunization against poliomyelitis. I. Protection with human gamma globulin against intramuscular inoculation, and combined passive and active immunization, Am. J. Hyg. 54: 132-143, 1951. MedlineGoogle Scholar7 Ibid.: II. The prophylactic effect of human gamma globulin on paralytic poliomyelitis in cynomolgus monkeys after virus feeding, Am. J. Hyg. 56: 78-89, 1952. MedlineGoogle Scholar8 Hammon WM: Evaluation of Red Cross gamma globulin as a prophylactic agent for poliomyelitis. 1. Plan of controlled field tests and results of 1951 pilot study in Utah, J. A. M. A. 150: 739-749, 1952. CrossrefMedlineGoogle Scholar9 Ibid.: 2. Conduct and early follow-up of 1952 Texas and Iowa-Nebraska studies, J. A. M. A. 150: 750-756, 1952. CrossrefMedlineGoogle Scholar10 Ibid.: Preliminary report of results based on clinical diagnoses, J. A. M. A. 150: 757-760, 1952. MedlineGoogle Scholar11 Hammon WM: Evaluation of Red Cross gamma globulin as a prophylactic agent for poliomyelitis, J. A. M. A. 151: 1272-1285, 1953. MedlineGoogle Scholar12 Report and supplementary report of Committee on Blood Banks to House of Delegates, American Medical Association, Denver, Colo., Dec. 2-5, 1952, J. A. M. A. 150: 1697-1698, 1952. Google Scholar13 Morgan IM: Immunization of monkeys with formalin inactivated virus, Am. J. Hyg. 48: 394, 1948. MedlineGoogle Scholar14 Schwerdt CE: Immunization of cotton rats with inactivated Lansing poliomyelitis virus. I. Inactivation by chemical agents, Am. J. Hyg. 53: 121-130, 1951. MedlineGoogle Scholar15 YoungnerWardSalk JSENJE: Studies on poliomyelitis viruses in cultures of monkey testicular tissue. I. Propagation of virus in roller tubes, Am. J. Hyg. 55: 291-300, 1952. MedlineGoogle Scholar16 Howe HA: Antibody response of chimpanzees and human beings to formalin-inactivated trivalent poliomyelitis vaccine, Am. J. Hyg. 56: 263, 2952. Google Scholar17 Salk JE: Studies in human subjects on active immunization against poliomyelitis. I. A preliminary report of experiments in progress, J. A. M. A. 151: 1081-1098, 1953. CrossrefMedlineGoogle Scholar18 Rivers TM: Vaccine for poliomyelitis (correspondence), J. A. M. A. 151: 1224, 1953. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 June 1953Volume 38, Issue 6Page: 1339-1344KeywordsPoliomyelitis ePublished: 1 December 2008 Issue Published: 1 June 1953 PDF downloadLoading ...

Quantitative studies of the virus-host relationship in chimpanzees after inapparent infection with Coxsackie viruses. I. The virus carrier state and the development of neutralizing antibodies.

Following oral administration of Coxsackie viruses (C viruses) to susceptible chimpanzees, these agents can be isolated from the throat for a period of approximately a week, from the blood for a few days, and from the stools for 2 to 3 weeks or even longer. Animals so infected respond with the formation of specific neutralizing antibodies which are maintained for at least 1 to 2 years. Such chimpanzees are immune when challenged orally with homologous strains of virus. They then excrete virus in the stools for 3 or 4 days (passive transfer); no virus can be recovered from the throats and blood of these animals, and neutralizing antibody levels remain unchanged. Animals immune to one antigenic type of C virus can be infected by feeding a different antigenic type. Following such a heterotypic challenge, virus can again be isolated from the throat, blood, and stools; neutralizing antibodies develop to the new strain. Antibodies to the Texas-1 type of C virus were already present in four chimpanzees upon their arrival in the laboratory from Africa. It was possible to set up intestinal carriage of the Texas-1 virus in these animals and to demonstrate a 10- to 100-fold increase in titer of neutralizing, as well as complement-fixing, antibody. Quantitative titrations of the amount of virus present in the stools and throat were performed. Immediately after the first feeding of virus relatively large amounts can be detected in the stools; the titer drops, but may be maintained for as long as 25 days at 10(-2) to 10(-3), furnishing evidence that virus multiplication has taken place. Virus in the throat reached the same order of magnitude at first as in the stools but there was a rapid decline to zero in a few days. The Ohio-1 virus differed from the others in that it persisted in the throat as long as in the stools, and in several instances reached a higher titer in the throat. Following homotypic challenge with all types, virus could be detected in the stools for only a relatively short period of time and at low concentration. Virus-neutralizing substances could not be detected in the stools or throat swabs of convalescent animals, at a time when their serum-neutralizing antibody titers were high. Under the limited conditions of the present experiments, C viruses had no effect on the infection of chimpanzees with three different antigenic types of poliomyelitis virus. Both poliomyelitis and C viruses set up independent infections without apparent interaction between them. No enhancement of the poliomyelitis infection took place, as was plain from the fact that none of the infected chimpanzees became paralyzed. a titration of Texas-1 C virus in four chimpanzees revealed that a suspension of infected tissue diluted to 10(6.0) could cause the development of the carrier state; accidental infection of control animals with other Coxsackie types indicated also that very little virus may be necessary to initiate infection. Seven distinct antigenic types of C virus were inoculated subcutaneously and intramuscularly at the same time into four chimpanzees. The response was the same as that following feeding; virus could be recovered from the throat, blood, and stools, and the animals developed neutralizing antibodies to all seven types of C virus. There was no detectable interference among the viruses. Cortisone did not bring about the reappearance of the virus excretion in chimpanzees previously infected and shown to be intestinal carriers of poliomyelitis and Coxsackie viruses.

EXPERIMENTAL STUDIES ON PASSIVE IMMUNIZATION AGAINST POLIOMYELITIS

Journal Article EXPERIMENTAL STUDIES ON PASSIVE IMMUNIZATION AGAINST POLIOMYELITIS: II. THE PROPHYLACTIC EFFECT OF HUMAN GAMMA GLOBULIN ON PARALYTIC POLIOMYELITIS IN GYNOMOLGUS MONKEYS AFTER VIRUS FEEDING Get access DAVID BODIAN DAVID BODIAN Search for other works by this author on: Oxford Academic PubMed Google Scholar American Journal of Epidemiology, Volume 56, Issue 1, July 1952, Pages 78–89, https://doi.org/10.1093/oxfordjournals.aje.a119543 Published: 01 July 1952 Article history Received: 08 April 1952 Published: 01 July 1952

Epizootic of Newcastle Disease in Pigeons and Studies on Transmission of the Virus

AS EARLY as 1927 Doyle in England reported that the pigeon was susceptible to Newcastle disease. He suggested that the susceptibility of the pigeon to intramuscular injection be used as a character in distinguishing Newcastle disease virus from that of fowl plague. Susceptibility of pigeons to the virus introduced by intravenous or intramuscular routes has been repeatedly shown (Picard, 1928; Cooper, 1931; Kylasamaier, 1931; Acevedo, 1933; Dobson, 1934; Kuppyswamy, 1937; Crawford, 1930; Manninger, 1936; and Pomeroy, 1948). Age has been reported to be a factor in susceptibility to infection, young pigeons being more susceptible than older birds (Picard, 1928). However, relative susceptibility of various types of doves as well as pigeons has been only superficially studied. Kaschula (1950) infected the laughing dove Streptopelia senegalensis (Stigmatopelia senegalensis) by intramuscular route but was unable to infect the ring dove Streptopelia capicola. Contact infection or infection by feeding virus has been reported in .