PubMed Health⌕ Search

Biomedical subjects

J B McCormick

Publications and source records attributed to J B McCormick.

At least 109 records · Page 6Linked to original sources

Lassa fever in children in Sierra Leone, West Africa.

A systematic study of Lassa fever in febrile children was undertaken over a four-year period, from August 1977 to August 1981, in the Eastern Province of Sierra Leone, West Africa. 479 patients were studied; of these, 245 had adequate specimens to confirm or exclude the laboratory diagnosis of Lassa fever. 51 cases of Lassa fever were identified (21% of patients from whom diagnosis was possible). Virus was isolated from 23 patients. All children had fever; cough and vomiting were present in over 60% of cases studied. The five to nine-year age group had the highest prevalence rate (41% of cases). Seasonal clustering occurred in April, May, and August. A significantly higher proportion of females than males had Lassa fever, a finding which remains to be explained. It is concluded that Lassa fever is a disease of significant concern in the paediatric age group.

Adolescent↗

Conservation of the 3' terminal nucleotide sequences of Ebola and Marburg virus.

The 3' RNA base sequences of several Marburg (MBG) and Ebola (EBO) virus isolates have been determined. A comparison of these 3' terminal noncoding sequences with those of other negative strand RNA viruses suggests a unique phylogenic niche for Marburg and Ebola viruses. The translation initiation site and 35 N-terminal amino acids of the 3' proximal coding gene of a Zaire strain of Ebola virus was predicted. In addition, putative leader RNA sequences preceding the first gene are discussed in terms of possible regulatory functions.

Base Sequence↗

Lassa virus hepatitis: a study of fatal Lassa fever in humans.

In order to explore the significance of a previous observation that the most important pathologic changes in fatal Lassa fever are hepatic, we have studied postmortem liver biopsies from 19 patients with fatal Lassa fever. We observed a vigorous macrophage response to cellular damage, but we found no evidence of lymphocyte infiltration in infected hepatic tissues. Using semi-quantitative estimates of liver cell damage, we found a wide range in the severity and progression of Lassa virus hepatitis in our fatal cases. We have classified for descriptive purposes three general nosopoeitic phases: active hepatocellular injury (less than 20% necrosis), continued damage and early recovery, and mitotic activity representing hepatic recovery. We conclude that the liver goes through cellular injury, necrosis and regeneration and any or all may be present at death. In no instance was the degree of hepatic damage sufficient to implicate hepatic failure, and all three phases were represented among our cases. We conclude that the hepatitis of Lassa fever in humans is not the primary cause of death.

Hepatitis, Viral, Human↗

Antiviral effect of ribavirin on Junin virus replication in vitro.

The effect of Ribavirin (1-beta-D-ribofuranosyl-1,2,4-triazole-3-carboxamide) on the replication in vitro of Junin virus, the causative agent of Argentine Hemorrhagic Fever (AHF), was examined. A concentration as low as 3.12 micrograms/ml of the drug inhibited the cytopathic effect observed five days post-infection (pi) on Vero cells. On the other hand, a concentration of 25 micrograms/ml reduced the virus yield and specific antigen formation to undetectable levels. This same concentration of Ribavirin prevented plaque formation under methylcellulose. The high sensitivity of Junin virus to Ribavirin in vitro, the low toxicity of the drug for mammals and the therapeutic effect observed on in vivo infections with other arenaviruses, makes Ribavirin a promising antiviral agent that deserves testing on AHF primate models before clinical trials are undertaken.

Animals↗

[Serological data on hemorrhagic fever with renal syndrome in Southeast Asia].

Using an indirect immunofluorescent test with Hantaan 76-118 and Puumala strains as antigens, antibodies against haemorrhagic fever with renal syndrome viruses were found for the first time in human in Laos and Viet-Nam and confirmed the previously published results in Thailand. These results suggest the existence of an Hantaan-related virus in these countries.

Antibodies, Viral↗

Early diagnosis of human Lassa fever by ELISA detection of antigen and antibody.

Sequential serum samples, beginning on the day of hospital admission, from three patients with Lassa fever were tested for the presence of Lassa-virus antigens and antibodies by means of an enzyme-linked immunosorbent assay. Lassa-virus antigens were detected in the first serum sample from each patient, thus providing an early definitive diagnosis. In contrast, seroconversion was not detectable by ELISA or indirect fluorescent antibody techniques until 3 days or more after admission. The antigen-detection ELISA has important advantages over conventional infectivity titrations; it takes only hours to carry out and can be accomplished safely, with beta-propiolactone-inactivated samples. Development of antibodies coincided with a decline in antigenaemia. All acute-phase Lassa-fever sera contained either antigen or IgM antibody, and most contained both, thus allowing early diagnosis with single serum samples. More extensive testing of these ELISA techniques is recommended in field hospitals where Lassa fever is endemic and rapid diagnostic tools are needed.

Antigens, Viral↗

Distinction between Bunyaviridae genera by surface structure and comparison with Hantaan virus using negative stain electron microscopy.

Ultrastructural studies of glutaraldehyde-fixed viruses of the Bunyaviridae were performed by negative-stain electron microscopy. The surface structure of viruses of each genus was compared with that of the other genera and with Hantaan virus, the prototype of a proposed new genus of Bunyaviridae. Viruses of each genus had a surface structure distinct for that genus. In addition, Hantaan virus had a surface structure composed of a grid-like pattern of morphologic subunits not previously described for animal viruses. Careful morphologic studies of suspected Bunyaviridae may be used in considering preliminary generic assignment. This study also supports the assignment of Hantaan-related viruses to a separate generic status within the Bunyaviridae.

Bunyaviridae↗

Descriptive analysis of Ebola virus proteins.

The virion proteins of two strains of Ebola virus were compared by SDS-polyacrylamide gel electrophoresis (PAGE) and radioimmunoprecipitation (RIP). Seven virion proteins were described; an L (180K), GP (125K), NP (104K), VP40 (40K), VP35 (35K), VP30 (30K), and VP24 (24K). The RNP complex of the virus contained the L, the NP, and VP30, with VP35 in loose association with them. The GP was the major spike protein, with VP40 and VP24 making up the remaining protein content of the multilayered envelope.

Animals↗

Serological and virological evidence of a Hantaan virus-related enzootic in the United States.

The first isolation of a Hantaan-related virus from a feral rat in the United States was made from a Rattus norvegicus caught in New Orleans. The strain, designated Tchoupitoulas virus, is antigenically related to, but distinct from, the prototype strain 76-118 of Hantaan virus and is the first Hantaan-like virus isolated from the pancreas of a naturally infected animal. Serosurveys of wild rodents from urban and rural areas in the United States indicated that Hantaan-related viruses infected urban rats in coastal and inland cities and infected five species of New World rodents in the western United States (Peromyscus maniculatus, Peromyscus difficilis, Peromyscus californicus, Neotoma mexicana, and Neotoma cinerea). Serosurveys disclosed no evidence of Hantaan-virus infection in rats in large-scale breeding colonies.

Animals↗

Kinetic study of platelets and fibrinogen in Lassa virus-infected monkeys and early pathologic events in Mopeia virus-infected monkeys.

The rhesus monkey, an established model of Lassa fever, was used to study hematologic and hemostatic aspects of Lassa fever and whether Mopeia (also known as Mozambique) virus induces any cellular damage in this model. Six days after subcutaneous injection of 10(3.48) plaque forming units (PFU) of Lassa virus (Josiah strain) one group of monkeys received an intravenous injection of 111In-labeled allogeneic platelets and another group received 125I-labeled alogeneic fibrinogen. Lassa virus-infected monkeys developed a severe clinical illness with high viremia and typical pathology. Lassa antigen was found in most tissues using a Lassa nucleocapsid-specific monoclonal antibody. Platelet counts remained within normal limits. Platelet and fibrinogen kinetics were similar in infected and control animals. Hematologic and hemostatic changes indicate that disseminated intravascular coagulation plays no role in this model of Lassa fever. Levels of plasma fibronectin were reduced in Lassa-infected monkeys. Mopeia virus-infected monkeys were normothemic, aviremic, and there was no detection of Mopeia antigen in any tissues using polyclonal or monoclonal antibodies. Mopeia virus was recovered from the spleen of one monkey. Mopeia virus was associated with hepatocellular and renal tubular damage.

Animals↗