PubMed Health⌕ Search

Biomedical subjects

S T Nichol

Publications and source records attributed to S T Nichol.

At least 55 records · Page 3Linked to original sources
PubMed1997

Isolation, genetic diversity, and geographic distribution of Bayou virus (Bunyaviridae: hantavirus).

Bayou hantavirus, previously implicated in human hantavirus pulmonary syndrome in Louisiana, was isolated from a rice rat (Oryzomys palustris) captured in Georgia. The presence of antibody among rice rats captured throughout the southeastern United States and the extent of diversity among the genetic variants of Bayou viruses suggest that the rice rat is the most likely natural reservoir of the virus and that both virus and host have probably co-evolved for some years.

Animals↗
PubMed1997

Molecular investigation of a multisource outbreak of Crimean-Congo hemorrhagic fever in the United Arab Emirates.

During the investigation of an outbreak of Crimean-Congo hemorrhagic fever (CCHF) in the United Arab Emirates (UAE) between 1994 and 1995, blood samples from suspected CCHF cases and ticks collected from livestock were tested for CCHF virus by antigen-capture ELISA and by a reverse transcription-polymerase chain reaction. Phylogenetic analysis of partial small (S) segment nucleotide sequences from four ticks and five human samples showed that with one exception, all the human and tick viruses clustered along with samples from Pakistan and Madagascar in one distinct lineage. Within this lineage, sequences from the UAE patients were identical or closely related to those from three Hyalomma spp. ticks obtained from livestock recently imported from Somalia. Another sequence from a UAE patient was more closely related to a CCHF virus from Nigeria. These data indicate that the 1994-1995 CCHF epidemic in the UAE was a multisource outbreak possibly associated with importation of CCHF virus-infected livestock and ticks.

Animals↗
PubMed1996

Ecological factors rather than temporal factors dominate the evolution of vesicular stomatitis virus.

Vesicular stomatitis New Jersey virus (VSV-NJ) is a rhabdovirus that causes economically important disease in cattle and other domestic animals in endemic areas from southeastern United States to northern South America. Its negatively stranded RNA genome is capable of undergoing rapid evolution, which allows phylogenetic analysis and molecular epidemiology studies to be performed. Previous epidemiological studies in Costa Rica showed the existence of at least two distinct ecological zones of high VSV-NJ activity, one located in the highlands (premontane tropical moist forest) and the other in the lowlands (tropical dry forest). We wanted to test the hypothesis that the viruses circulating in these ecological zones were genetically distinct. For this purpose, we sequenced the hypervariable region of the phosphoprotein gene for 50 VSV-NJ isolates from these areas. Phylogenetic analysis showed that viruses from each ecological zone had distinct genotypes. These genotypes were maintained in each area for periods of up to 8 years. This evolutionary pattern of VSV-NJ suggests an adaptation to ecological factors that could exert selective pressure on the virus. As previous data indicated an absence of virus adaptation to factors related to the bovine host (including immunological pressure), it appears that VSV genetic divergence represents positive selection to adapt to specific vectors and/or reservoirs at each ecological zone.

Animals↗
PubMed1996

Isolation and characterization of Whitewater Arroyo virus, a novel North American arenavirus.

Rodents are principal hosts for each of the well-characterized arenaviruses. Prior to the present study, Tamiami (TAM) virus was the sole arenavirus known to be indigenous to North America; it has been isolated only from southern Florida where its primary host is the cotton rat Sigmodon hispidus. Recently, arenavirus antibody was found in Neotoma albigula woodrats collected from the southwestern United States. The purpose of the present study was to isolate and characterize the arenavirus associated with N. albigula. Three isolates of a novel arenavirus (proposed name "Whitewater Arroyo," WWA) were recovered from two arenavirus antibody-positive N. albigula collected from Whitewater Arroyo in McKinley County, New Mexico. Two-way serologic tests indicated that WWA virus is antigenically distinct from other arenaviruses but most closely related to TAM virus. Phylogenetic analysis of nucleocapsid protein gene sequence data showed that WWA virus is a novel arenavirus that is genetically most closely related to TAM virus. The recovery of WWA virus from antibody-positive N. albigula suggests that WWA virus infection in this species can be chronic and thus that N. albigula is a reservoir host of the virus.

Animals↗
PubMed1996

Sin Nombre virus mRNA synthesis.

Sin Nombre (SN) virus is the major etiologic agent of hantavirus pulmonary syndrome, a severe respiratory disease with high mortality. Like other hantaviruses, SN virus causes an inapparent chronic infection of the natural rodent reservoir and tends to grow slowly and produce little cytopathic effect even in highly susceptible Vero E6 tissue culture cells. An electrochemiluminescent quantitative PCR approach was developed to allow examination of SN virus RNA transcription in synchronously infected cells. Although virion particles contain equimolar ratios of the three negative-strand genome RNA segments (S, M, and L), rates and levels of accumulation of the corresponding N, GPC, and L viral mRNAs varied. The smallest mRNA (N) was detectable earliest and plateaued at the highest level, where as the largest mRNA (L) appeared latest and at the lowest plateau level. In addition, all three mRNAs were found to share a common 5' capped primer initiation mechanism, but appeared to have different mRNA termination mechanisms. The N mRNA 3' terminus mapped to position 1435 on the S segment, in close proximity to a CCC-rich suspected transcription termination motif. The GPC mRNA 3' terminus contained a poly(A) tall and mapped to a U8 transcription termination-polyadenylation motif reminiscent of those seen in other negative-strand RNA viruses. Finally, the L mRNA 3' terminus appeared identical to the L segment antigenome 3' terminus.

Animals↗
PubMed1996

Genetic characterization and phylogeny of Sabiá virus, an emergent pathogen in Brazil.

Sabiá virus, one of five arenaviruses from South America known to cause hemorrhagic fever in humans, emerged in 1990 when it was isolated from a fatal case in Sao Paulo, Brazil. Subsequently, it has caused two laboratory-acquired infections. Its natural distribution and host are still unknown. Using viral RNA and multiple polymerase chain reaction products as templates, the nucleotide sequence of the small (S) RNA segment of Sabiá virus, which codes for the nucleocapsid (N) and glycoprotein precursor, was determined. This virus shares an ambisense genome in common with other arenaviruses, although it has a unique predicted three stem--loop structure in the S RNA intergenic region. Phylogenetic analysis of a portion of the N gene sequence confirmed that Sabiá virus is distinct from all other members of the Arenaviridae and shares a progenitor with Junin, Machupo, Tacaribe, and Guanarito viruses.

Amino Acid Sequence↗
PubMed1996

The phylogeny of New World (Tacaribe complex) arenaviruses.

Several New World (Tacaribe complex) arenaviruses (Arenaviridae) are known to cause severe hemorrhagic disease in humans. Phylogenetic reconstruction of the Tacaribe complex arenaviruses previously has been limited by the relative scarcity of sequence data for arenavirus genomes. In the present study, oligonucleotide primers were designed based on conserved regions of the nucleocapsid (N) protein gene and then used to amplify, by reverse transcription--polymerase chain reaction, a 613-to 649-nucleotide region of the N gene of all known Tacaribe complex arenaviruses. This has allowed completion of the first detailed genetic characterization and phylogenetic analysis of all known members of the Tacaribe complex. These viruses formed three lineages. Lineage A contained Flexal, Parana, Pichinde, and Tamiami viruses; lineage B contained Amapari, Guanarito (GUA), Junin (JUN), Machupo (MAC), Sabia (SAB), and Tacaribe viruses. Latino and Oliveros viruses occupied lineage C. The highly pathogenic Tacaribe complex arenaviruses (GUA, JUN, MAC, SAB) were all members of lineage B, suggesting the possibility that the highly pathogenic phenotype is the result of evolutionary radiation from a common ancestor. The approach described here provides a rapid method for characterization of novel Tacaribe complex arenaviruses and may provide clues as to their potential public health importance.

Arenaviruses, New World↗
PubMed1996

The virion glycoproteins of Ebola viruses are encoded in two reading frames and are expressed through transcriptional editing.

In late 1994 and early 1995, Ebola (EBO) virus dramatically reemerged in Africa, causing human disease in the Ivory Coast and Zaire. Analysis of the entire glycoprotein genes of these viruses and those of other EBO virus subtypes has shown that the virion glycoprotein (130 kDa) is encoded in two reading frames, which are linked by transcriptional editing. This editing results in the addition of an extra nontemplated adenosine within a run of seven adenosines near the middle of the coding region. The primary gene product is a smaller (50-70 kDa), nonstructural, secreted glycoprotein, which is produced in large amounts and has an unknown function. Phylogenetic analysis indicates that EBO virus subtypes are genetically diverse and that the recent Ivory Coast isolate represents a new (fourth) subtype of EBO virus. In contrast, the EBO virus isolate from the 1995 outbreak in Kikwit, Zaire, is virtually identical to the virus that caused a similar epidemic in Yambuku, Zaire, almost 20 years earlier. This genetic stability may indicate that EBO viruses have coevolved with their natural reservoirs and do not change appreciably in the wild.

Animals↗
PubMed1996

Oliveros virus: a novel arenavirus from Argentina.

During the past few decades several newly recognized rodent-borne arenaviruses have been shown to be associated with severe hemorrhagic fever cases in South America. Changes in ecology and farming practices throughout the region have increased the concern over the potential public health threat posed by such emerging virus diseases. Oliveros (OLV) virus is a recently discovered arenavirus of the rodent Bolomys obscurus in Argentina. Genetic analysis of the small genomic RNA segment, which encodes the nucleocapsid protein and the envelope glycoproteins, shows that Oliveros is a novel, phylogenetically distinct member of the Arenaviridae family which differs in nucleotide sequence from the previously characterized members by approximately 35% or more. Despite this level of diversity, OLV virus possesses the same ambisense genome structure and many overall RNA and protein features in common with other arenaviruses. These data represent an important first step in the development of specific immunological and PCR diagnostic reagents to allow assessment of the prevalence and disease potential of this virus.

Animals↗
PubMed1996

Hantavirus pulmonary syndrome in Florida: association with the newly identified Black Creek Canal virus.

Hantavirus pulmonary syndrome (HPS) is a recently recognized viral zoonosis. The first recognized cases were caused by a newly described hantavirus. Sin Nombre virus (previously known as Muerto Canyon virus), isolated from Peromyscus maniculatus (deer mouse). We describe a 33-year-old Floridian man who resided outside the ecologic range of P maniculatus but was found to have serologic evidence of a hantavirus infection during evaluation of azotemia associated with adult respiratory distress syndrome. Small mammal trapping conducted around this patient's residence demonstrated the presence of antihantaviral antibodies in 13% of Sigmodon hispidus [cotton rat). Serologic testing using antigen derived from the Black Creek Canal hantavirus subsequently isolated from this rodent established that this patient was acutely infected with this new pathogenic American hantavirus. HPS is not confined to the geographical distribution of P maniculatus and should be suspected in individuals with febrile respiratory syndromes, perhaps associated with azotemia, throughout the continental United States.

Acute Kidney Injury↗
PubMed1996

Hantavirus pulmonary syndrome: the first 100 US cases.

In the spring of 1993, hantavirus pulmonary syndrome (HPS) "emerged" in the southwestern United States, where a multiagency investigation led to the rapid description of this new clinical entity and its etiology. Analysis of the first 100 US cases identified showed that the disease was distributed in 21 states, had gone unrecognized since at least 1959, and had a distinct spring-early summer seasonality. Of the infected persons, 54% were male; 63% were Caucasian, 35% were Native American, and 2% were African American. The average age of case-patients was 34.9 years, and 8 were children or adolescents aged < or = 16 years. The overall case-fatality rate was 52%. There was a 91% concordance among serologic, immunohistochemical, and molecular results. HPS in the United States is caused by at least three newly described pathogenic hantaviruses, each of which has a distinct rodent host, and cases of HPS have been recently recognized in Canada and South America. National surveillance of this sporadic disease remains essential for further defining the epidemiology and clinical spectrum.

Adolescent↗
PubMed1996

Direct genetic detection of Dobrava virus in Greek and Albanian patients with hemorrhagic fever with renal syndrome.

Blood samples were collected from an Albanian and a Greek patient with hemorrhagic fever with renal syndrome and tested by reverse transcriptase-polymerase chain reaction. The genetic detection assay amplified hantavirus-specific DNA fragments from RNA extracted from the blood of the patients; nucleotide sequence analysis revealed that the causative agent of the disease was Dobrava virus. These findings suggest that Dobrava virus (which was originally isolated from the lungs of an Apodenws flavicollis mouse in Slovenia) is endemic throughout the Balkan States and causes overt human disease.

Adult↗
PubMed1996

Occurrence of hantavirus within the rodent population of northeastern California and Nevada.

These studies were initiated to determine the prevalence and hosts of hantaviruses within the rodent population of Nevada and northeastern California. A total of 1,867 rodents were collected, sexed, weighed, identified, and tested by enzyme-linked immunosorbent assay for the presence of antibody against hantavirus nucleocapsid. The primary hosts for hantaviruses in this region were found within the family Muridae (Peromyscus maniculatus. Reithrodontomys megalotis. and Microtus montanus). Studies over time of animals within a defined geographic area indicated that animals with hantavirus antibody are not distributed uniformly over the rodent population in a specific area but were found in foci spanning a distance of only several hundred meters. The antibody prevalence in a given geographic area remained relatively constant with repeated sampling of between 0% and 30%. These data support the hypothesis that rodents within the family Muridae are the primary reservoir for hantaviruses, and the primary risk to biologists for exposure to hantavirus is by contact with members of this family.

Animals↗
PubMed1995

Naturally occurring Sin Nombre virus genetic reassortants.

Genetic reassortment has been shown to play an important role in the evolution of several segmented RNA viruses and in the epidemiology of associated diseases. Sin Nombre (SN) virus is the cause of hantavirus pulmonary syndrome throughout the western United States. Like other hantaviruses, it possesses a genome consisting of three negative-sense RNA segments, S, M, and L. Recent analysis has demonstrated the presence of at least three different hantaviruses in Nevada and eastern California, including SN, Prospect Hill-like, and El Moro Canyon-like viruses. In addition, two distinct lineages of SN virus can be found in Peromyscus maniculatus rodents (sometimes in close proximity) trapped at study sites in this region. Data obtained by phylogenetic analysis of sequence differences detected among the S, M, and L genome segments of these SN viruses are consistent with reassortment having taken place between SN virus genetic variants. The results suggest that M (and to a lesser extent S or L) genome segment flow occurs within SN virus populations in P. maniculatus in this region. No reassortment was detected between SN virus and other hantavirus types present in the area. This finding suggests that as genetic distance increases, the frequency of formation of viable reassortants decreases, or that hantaviruses which are primarily maintained in different rodent hosts rarely have the opportunity to genetically interact.

Animals↗
PubMed1995

Coexistence of several novel hantaviruses in rodents indigenous to North America.

Three genetically distinct members of the Hantavirus genus have been detected in Nevada rodents by RT-PCR and nucleotide sequence analysis. These include Sin Nombre (SN), El Moro Canyon (ELMC), and Prospect Hill (PH)-like viruses which are primarily associated with Peromyscus maniculatus (deer mouse), Reithrodontomys megalotis (western harvest mouse), and Microtus spp. (voles), respectively. Although this region of the United States is ecologically diverse, rodents infected with different hantaviruses appear to coexist in several different geographical and ecological zones. In two widely separated states, Nevada and North Dakota, PH-like viruses are present in three different species of vole. In addition, ELMC-like virus has been detected in both R. megalotis and M. montanus (mountain vole). SN virus is a cause of hantavirus pulmonary syndrome throughout much of the United States. SN virus RNA is found in 12.5% of P. maniculatus in Nevada and eastern California. Two lineages of SN virus coexist in this region and differ from SN viruses originally found in infected rodents in New Mexico, Arizona, and Colorado. These data show the complexity of hantavirus maintenance in rodents. Distinct hantaviruses or virus lineages can coexist either in different or the same rodent species and in either different or the same geographic or ecological zones.

Animals↗
PubMed1995

Genetic and serologic analysis of Black Creek Canal virus and its association with human disease and Sigmodon hispidus infection.

Black Creek Canal (BCC) virus is a newly identified virus associated with hantavirus pulmonary syndrome (HPS) in the southeastern United States. Nucleotide sequences were determined for the complete S and M and partial L genomic segments of a BCC virus isolate. Phylogenetic analysis indicates that each of the virus segments is unique, and there is no evidence of genetic reassortment having occurred between this and other previously characterized hantaviruses. All hantavirus-seropositive, wild-caught Sigmodon hispidus which were tested by polymerase chain reaction for the presence of BCC virus RNA were found to be positive, consistent with a chronic virus infection. This finding, together with serologic evidence, confirms S. hispidus as the primary rodent reservoir of this virus. Nucleotide sequence analysis of these PCR products indicates that BCC virus is genetically diverse and may pose a public health threat throughout much of the extensive range of this rodent species. Immunoprecipitation analysis demonstrated the presence of G1-, G2-, and N-specific antibodies in sera from BCC virus-infected patients with HPS and naturally infected S. hispidus. Comparison of the patterns of protein immunoprecipitation obtained with human acute- and convalescent-phase sera suggests that G1- and G2-specific antibodies increase relative to N-specific antibodies during the course of infection. The ratio of G1 to N protein immunoprecipitation by rodent or human acute-phase sera allowed differentiation of BCC and Sin Nombre virus infections.

Amino Acid Sequence↗
PubMed1995

Rabies virus glycoprotein gene contains a long 3' noncoding region which lacks pseudogene properties.

Analysis of a limited number of laboratory strains of rabies virus had demonstrated the presence of a genome region bounded by two transcription termination and polyadenylation-like (TTP) signals (approximately 400 to 450 nucleotides apart) which was located between the end of the glycoprotein (G) coding sequence and the beginning of the L polymerase coding sequence. Although this region had been suggested to represent a remnant or pseudogene (psi), no detailed analysis had been carried out to examine this possibility. Here we present the nucleotide sequence analysis of this genome region for several laboratory rabies virus strains and a large number of diverse rabies viruses detected directly in brain tissue of naturally infected animals. Only one distinct lineage of the laboratory strains and none of the wild-type rabies viruses contained the upstream TTP-like signal, indicating that only the downstream TTP motif is the authentic G mRNA transcription termination and polyadenylation and signal. Phylogenetic analysis of sequence differences provided no evidence of laboratory strains containing the two TTP-like signals being ancestral to any of the viruses possessing only the downstream TTP sequence motif. These data indicate that this region of the rabies virus genome encodes a G mRNA with a long 3' noncoding region with no evidence of a pseudogene.

Animals↗