Biomedical subjects

T O Harry

Publications and source records attributed to T O Harry.

23 records · Page 2Linked to original sources

PubMed1981

Optimal age for vaccinating Nigerian children against measles. I. Neonatal antibody profile and subsequent susceptibility to measles.

The decline of maternally acquired haemagglutination inhibiting antibodies against measles virus in Nigerian children born in Lagos was studied. At birth all the 303 children whose cord blood serum was tested had measurable antibodies. The antibody titre remained detectable in all the children up to four months of age, and in over 90% at five months of age. At six months 65% of the children were without detectable antibodies. At seven and eight months the proportion of children without measurable antibodies was reduced to 50% and 42% respectively, indicating a slight but progressive improvement in the immune status of the children. These findings provide a serological basis for starting anti-measles immunization of Nigerian children at six months.

Age Factors↗

PubMed1981

Optimal age for vaccinating Nigerian children against measles. II. Seroconversion to measles vaccine in different age groups.

Ninety-eight children between five and nine months were given measles vaccine. Bloodsamples were taken before and again six to eight weeks after immunization and tested for haemagglutination inhibition antibodies to measles virus. It was found that the sero-conversion rate was significantly lower (p less than 0.05) in infants under seven months than over this age. The results suggest that although some immunized at six months of age show seroconversion, the proportion is too small to justify extensive immunization at this age. It is proposed that children in Lagos should be immunized from the age of eight to nine months.

Age Factors↗

PubMed1978

Expression of vaccinia virion surface tubule protein as a virus specific cell surface antigen.

The sequential expression of a vaccinia virus specific antigen on the surface of infected cells has been followed by 125I-labelled anti-vaccinia IgG. After an initial drop (during the first 30 minutes of infection) the amount of viral antigen at the cell surface increased steadily for the 12 hours tested. The expression of the antigen was found to depend on protein and RNA synthesis from the start, but dependent on DNA synthesis only after 4 hours. The senitivity of the phenomenon to ultraviolet light irradiation of the virus suggests that the genetic information needed for the expression of the antigen resides in the viral genome. The antigen has been identified as the virion surface tubule, a tubule-like structure on the surface of the intact virion. It is known that vaccinia virus infection of cells starts with the fusion of the virion envelope with the host plasma membrane. It is here proposed that initially tubule from input virus is detected as viral antigen on the cell surface. Subsequently, virus tubule protein synthesised de novo migrates and is detectable as the virus specific cell surface antigen.

Antigens, Surface↗

PubMedDate not supplied

Urban yellow fever epidemic in western Nigeria, 1987.

A large epidemic of urban yellow fever occurred in April and May 1987 in Oyo State, western Nigeria. The principal vector was Aedes aegypti, breeding in domestic water containers. The 1987 outbreak followed an epidemic of sylvatic yellow fever in eastern Nigeria the previous year, and probably resulted from introduction of the virus by viraemic travellers. The outbreak in Oyo State ended in early July, by which time 805 cases and 416 deaths had been officially notified. However, surveys of 3 villages in the epicentre, a region with over 4 million inhabitants, indicated an infection rate of approximately 20%, a clinical attack rate of 2.9% and a mortality rate of 0.6%, suggesting that the true incidence of cases and deaths far exceeded the official reports. Yellow fever virus was isolated from persons with fully developed yellow fever as well as mild febrile illness. One virus isolate was made from blood of an individual with mild illness, who had received 17D vaccine 5 d earlier; monoclonal antibody analysis showed that the isolate was a wild-type virus. Larval indices of Ae. aegypti were very high; however, low vector competence of the Ae aegypti population may have provided a constraint on spread of the epidemic. In late 1987 a third epidemic appeared in Niger State, northern Nigeria, with 644 reported cases and 149 deaths. The vector(s) involved is (are) unknown.

Adolescent↗

PubMedDate not supplied

A survey for antibodies to Lassa virus among health workers in Nigeria.

A study was conducted among 552 health workers at 6 health facilities in Nigeria. Lassa virus immunoglobulin (Ig) G antibody was detected in 12.3%, using an enzyme-linked immunosorbent assay. Antibody prevalence in the 6 health centres ranged from 1.2% to 27.3%. Prevalences were higher in primary and secondary health facilities than in tertiary centres. Seroprevalences ranged from 1.7% to 23.7% among different occupational groups of health workers; the highest observed antibody prevalence was among ward aids. Lassa virus IgM antibody, indicating recent infection, was present in 6 of the health workers, 5 of whom were ward aids and one was a nurse. All of the health workers with specific IgM came from a single facility in Lafia, sampled during an outbreak of Lassa fever.

Antibodies, Viral↗