Evaluation of the polymerase chain reaction for diagnosis of herpes simplex virus encephalitis.

Cerebrospinal fluid samples from 257 patients with suspected herpes simplex virus encephalitis were prospectively analyzed by herpes simplex virus polymerase chain reaction. The polymerase chain reaction indicated herpes simplex virus encephalitis in 9 serologically proven cases and in 14 additional patients. Increased polymerase chain reaction signals were observed together with more severe neurological symptoms (P < 0.01) and within the first days of acyclovir treatment (P < 0.05).

Molecular evidence for the origin of the widespread Venezuelan equine encephalitis epizootic of 1969 to 1972.

Venezuelan equine encephalitis (VEE) virus is a mosquito-borne pathogen that has caused encephalitis in equine species and humans during sporadic outbreaks in the western hemisphere. The last, and most widespread, VEE outbreak occurred in South America, Central America, Mexico and the U.S.A. (Texas) during 1969 to 1972. We have cloned and sequenced the genome of a virulent VEE subtype I-AB virus, strain 71-180, isolated in Texas in 1971. Thirty-four nucleotide differences were detected between the genome of 71-180 virus and that of the subtype I-AB Trinidad donkey (TRD) virus isolated during the 1943 VEE epizootic in Trinidad. Fifteen nucleotide changes occurred in the non-structural genes, 16 in the structural genes and three in the 3' non-coding region. Only six of the nucleotide differences resulted in amino acid substitutions: one change in each of non-structural proteins nsP1 and nsP3, two in the E2 envelope glycoprotein, one in the 6K polypeptide and one in the E1 envelope glycoprotein. The close genetic relationship between 71-180 virus and TRD virus, commonly used for production of formalin-inactivated VEE vaccines, suggests that incompletely inactivated virulent vaccine virus may have been the source of this and other VEE outbreaks. Use of formalized virulent virus was discontinued during the 1969 to 1972 panzootic. No VEE epizootics have been reported since the introduction of the live attenuated TC-83 vaccine virus.

Molecular evidence for the origin of the widespread Venezuelan equine encephalitis epizootic of 1969 to 1972

Venezuelan equine encephalitis (VEE) is a mosquito-borne pathogen that has caused encephalitis in equine species and humans during sporadic outbreaks in the western hemisphere. The last, and most widespread, VEE outbreak occurred in South America, Central America, Mexico and the U.S.A. (Texas) during 1969 to 1972. We have cloned and sequenced the genome of a virulent VEE subtype I-AB virus, strain 71-180, isolated in Texas in 1971. Thirty four nucleotide differences were detected between the genome of 71-80 virus and that of subtype I-AB Trinidad donkey (TRD) virus isolated during the 1943 VEE epizootic in Trinidad. Fifteen nucleotide changes occurred in the non-structural genes, 16 in the structural genes and three in the 3' non-coding region. Only six of the nucleotide diferences resulted in amino acid substitutions: one change in each of non-structural proteins nsP1 and nsP3, two in the E2 envelope glycoprotein, one in the 6K popypeptide and one in the E1 envelope glycoprotein. The close genetic relationship between 71-180 virus and TRD virus, commonly used for production of formalin-inactivated VEE vaccines, suggests that incompletely inactivated virulent vaccine virus may have been the source of this and other VEE outbreaks. Use of formalized virulent virus was discontinued during the 1969 to 1972 panzootic. No VEE epizootics have been reported since the introduction of the live attenuated TC-83 vaccine virus (AU)

[Epidemiology of encephalitis caused by arbovirus in the Brazilian Amazonia]. / Epidemiologia das encefalities por arbovírus na Amazônia brasileira.

An overview of ecological, epidemiological and clinical findings of potential arthropod-borne encephalitis viruses circulating in the Amazon Region of Brazil are discussed. These viruses are the Eastern Equine Encephalitis (EEE), Western Equine Encephalitis (WEE), St. Louis Encephalitis (SLE), Mucambo (MUC) and Pixuna (PIX). These last two are subtypes (III and IV) of Venezuelan Equine Encephalitis virus. The areas of study were the highways and projects of development, as well as places where outbreaks of human diseases caused by arboviruses had been detected. These viruses are widespread in all Amazonia, and at least four of them, EEE, WEE, SLE and MUC are pathogenic to man. EEE and WEE infections were detected by serology, while SLE and MUC by either serology and virus isolation. The PIX virus has the lowest prevalence and, it was isolated in only a few cases, one being from a laboratory infection. Wild birds are the main hosts for all these viruses, except MUC, whose major hosts are rodents. The symptoms presented by infected people were generally a mild febrile illness. Although, jaundice was observed in two individuals from whom SLE was isolated. A comparison of the clinical symptoms presented by the patients in the Amazon Region and other areas of America, especially in the USA is made. In Brazilian Amazon region epidemics have not been detected although, at least, one EEE epizootic was recorded in Bragança, Para State, in 1960. At that time, of 500 horses that were examined 61% were positive to EEE by HI and of them 8.2% died. On the other hand, SLE has caused four epizootics in a forest near Belem. Wild birds and sentinel monkeys were infected, but no human cases were reported.

Astrogliosis in von Economo's and postencephalitic Parkinson's diseases supports probable viral etiology.

A marked generalized astrogliosis was observed in the frontal and temporal white matter from a case of von Economo's disease and another of postencephalitic Parkinson's disease, which areas were otherwise devoid of any other demonstrable microscopic lesions. No similar astrocytic reaction of any severity was observed in the same areas in a number of other brain diseases or controls, except when other kinds of lesions were present in the same section, with reactive astrocytes being present within the primary or defining lesion or immediately close by. The marked astrogliosis in von Economo's and postencephalitic Parkinson's diseases in areas "distant" from the primary lesions seeming to indicate extensive pathological involvement, added to the strong qualitative and quantitative similarity of this reaction to that observed in concurrently studied cases of encephalitides caused by the human immunodeficiency virus, lend further factual support to the hypothesis of a viral etiology, albeit unspecified, in both von Economo's and postencephalitic Parkinson's diseases.

[Acute non-suppurative encephalitis in children]. / Akut non-suppurativ encefalit hos børn.

From July 1973 to January 1988, 66 children aged from three months to 14 years, 36 boys and 29 girls, were seen at the Central Hospital, Viborg, with acute encephalitis. In 25 cases the encephalitis was caused by mumps, in eight by measles, in six by chicken pox, one by herpes simplex, one by RS-virus, and one by mycoplasma. One case was seen after vaccination, one after infection and in 22 cases the cause of the encephalitis remained unknown. Sequelae were seen in 17 cases. The risk of encephalitis after mumps, measles, and rubella is an important argument for the use of MMR-vaccination and the risk of encephalitis after chickenpox may justify a vaccination campaign against chickenpox.

[New types of virus infections of domestic animals in the German Democratic Republic. 4. Tahyna virus infections--a review]. / Für die DDR neuartige Virusinfektionen der Haustiere. 4. Mitteilung: Die Tahyna-Virusinfektion--ein Uberblick.

A general account is given in this paper of history, incidence, pathogen properties, morphogenesis, isolation, and culturing of Tahyna virus. Reference is also made to methods for detection, host spectrum, immunity, epizootiology, pathogenesis, and clinical symptoms in man and animals and also to aspects relating to pathological anatomy as well as to regular and differential diagnosis.

Influenza caused epidemic encephalitis (encephalitis lethargica): the circumstantial evidence and a challenge to the naysayers.

Circumstantial evidence implicates the influenza virus as the cause of epidemic encephalitis. Arguments used to refute influenza as the causative agent are examined and a challenge is made to naysayers to implicate a viral agent other than influenza.

Serologic prevalence of caprine arthritis-encephalitis virus in California goat dairies.

Fifty-three percent of goats in 13 California goat dairies had antibodies to caprine arthritis-encephalitis virus (CAEV), as determined by agar-gel immunodiffusion. Those goat dairies that reared kids on pasteurized milk had a lower seroprevalence than those that did not. Age, rearing kids on unpasteurized milk, and the presence of large joints were associated with antibodies to CAEV. Breed was associated with seroreactivity, but the association was confounded by other factors. Sex was not associated with antibodies to CAEV. The relationship between age and antibodies to CAEV was observed for goats reared on pasteurized or unpasteurized milk, which indicated that continued horizontal (contact) transmission may be important on these dairies and limited the effect of a pasteurized rearing program on control of CAEV infection.

Human and viral gene detection in routine paraffin embedded tissue by in situ hybridisation with biotinylated probes: viral localisation in herpes encephalitis.

A simple reproducible protocol for detecting multiple copy human genes and viral DNA in routine formalin fixed paraffin embedded tonsil and brain, by in situ hybridisation with biotinylated probes, is described. The protocol consists of digestion of formalin fixed paraffin sections, with 0.4% pepsin in 0.01 M hydrochloric acid for one hour at 37 degrees C, followed by hybridisation with biotinylated probes. The biotinylated probes used for establishing the conditions for in situ localisation of DNA were total placental DNA (TG1), pHY 2.1 (a Y chromosome probe), and herpes simplex virus I and II. In human male tonsil TG1 labelled all nuclei and pHY 2.1 reacted only with nuclear Y bodies. In herpes encephalitis the virus was detected in some glial cells and neurones.

Experimental La Crosse virus infection of red fox (Vulpes fulva), raccoon (Procyon lotor), opossum (Didelphis virginiana), and woodchuck (Marmota monax).

Susceptibility to infection, resulting viremia and antibody responses, and potential to provide infectious blood meals for Aedes triseriatus were determined and compared for the red fox (Vulpes fulva), raccoon (Procyon lotor), and opossum (Didelphis virginiana) exposed to La Crosse (LAC) virus transmitted by mosquitoes, Ae. triseriatus. Woodchucks (Marmota monax) were infected with LAC virus by needle and syringe. All 5 red foxes became viremic following the bite of a single LAC virus-infected female Ae. triseriatus. Maximum viremia titers were at or above the threshold of infection for Ae. triseriatus in 4 of 5 red foxes for 1-3 days. Biological transmission of LAC virus from infected red foxes to chipmunks (Tamias striatus) was accomplished by Ae. triseriatus. Neutralizing antibody titers in red foxes peaked between day 13 and 27 and were still detectable 3 months post-infection. Woodchucks appear to be efficient amplifiers of LAC virus. Three of 4 inoculated woodchucks became viremic. Maximum viremia titers were consistently above the experimentally determined threshold of infection for Ae. triseriatus. Raccoons and opossums were not as susceptible to LAC virus infection as were red foxes or woodchucks. Only 1 of 5 raccoons became viremic. The viremia titer was low and was detected on only 1 day. Four of 5 raccoons developed LAC virus-neutralizing antibody titers, however. None of the opossums became viremic and only 2 developed LAC virus-neutralizing antibody titers.

California serogroup viruses in New York State: the role of subtypes in human infections.

The roles of various subtypes of the California serogroup viruses as infectious agents and as neuropathogens were evaluated by using the plaque reduction neutralization test. Sera from 394 patients with central nervous system (CNS) infections during 1971-1982 and from 501 persons without CNS manifestations were studied. Jamestown Canyon (JC) and La Crosse (LAC) viruses were found to have been common infectious agents in New York State for at least 16 years. JC virus was the prevalent indicated agent in patients with antibody to California serogroup viruses in screening tests (62 of 93 cases), followed by LAC virus (11 cases), snowshoe hare (2 cases), and trivittatus (1 case). In the remaining 17 patients the subtype was undetermined. LAC virus appears to be more pathogenic for children and to produce more serious illness, as judged by the frequent clinical diagnosis of encephalitis. JC virus affects mainly adults, and meningitis was the most common diagnosis. JC virus appears to cause a stronger neutralizing antibody response than does LAC virus, with a longer persistence of high levels of antibody. Some cases of JC virus infection may have been missed in the past due to the choice of a LAC-like isolate from New York State as the sole antigen in hemagglutination-inhibition (HI) screening tests. Comparison of the HI test and a single-dilution neutralization assay for screening for the two major subtypes, JC and LAC, indicated that the latter procedure is more broadly reactive and is less likely to miss cases if only one test antigen is used.

Neutralizing and non-neutralizing monoclonal antibodies to the E2 glycoprotein of Semliki Forest virus can protect mice from lethal encephalitis.

Two monoclonal antibodies (UM 4.2 and UM 5.1) directed against the glycoprotein E2 of Semliki Forest virus (SFV) are described; both belong to the IgG2a isotype but are of different idiotype. Analysis employing isoelectric focusing resulted in different focusing patterns for both monoclonals (UM 4.2, pI 8; UM 5.1, pI 7.2). They further differed in their ability to neutralize virus. The UM 4.2 antibodies were inactive in neutralization, while the UM 5.1 antibodies exceeded conventional mouse hyperimmune serum in this respect. Both monoclonal antibodies, however, were able to protect mice passively from a lethal infection with SFV. Based on the amount of protein, the UM 5.1 antibodies were 100-fold more effective than the UM 4.2 antibodies in mouse protection tests.