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PubMed1993

Arbovirus infections of humans in high-risk areas of south-eastern Australia: a continuing study.

OBJECTIVES: To determine the current immune status of high-risk populations of New South Wales and Victoria to the arboviral pathogens, Murray Valley encephalitis (MVE) and Kunjin (KUN) viruses, which are associated with Australian encephalitis (AE), and Ross River (RR) and Kokobera (KOK) viruses which are associated with polyarthritis. Further, to estimate seroconversion rates to these viruses in high-risk populations over the 10-year period 1981-1991. DESIGN AND STUDY POPULATION: Blood was taken from 2873 permanent residents, children and adults from previously identified high-risk areas in western NSW and northern Victoria. Samples were tested by the haemagglutination-inhibition (HI) test for antibodies to the four viruses. All sera were also tested for MVE and KUN antibodies by the more specific neutralisation test (NT). Ninety-five of the subjects had been seronegative when sampled 10 years previously. RESULTS: Age standardised prevalence rates for flavivirus HI antibodies (MVE, KUN, KOK) ranged from 66% (Bourke) to 15% (Forbes), and were similar to those observed 10 years previously. However, specific NT antibodies to MVE and KUN were uncommon in all districts except Bourke, indicating a very high level of susceptibility to Australian encephalitis, should a fresh epidemic occur. Whereas KUN virus seems enzootic in NSW and Victoria, MVE did not appear to have been present since the last outbreak in 1974, even in Bourke. Flavivirus antibody rates (as detected by the broadly reactive HI test) greatly exceeded those specifically attributable to MVE and KUN (NT test) or KOK, leading to the speculation that unidentified flaviviruses are responsible for most human infections. Ross River virus antibody prevalence rates exceeded those of flaviviruses in all districts, ranging from 72% (Bourke) to 25% (Cohuna), and were uniformly higher than those observed in 1981. Ten-year seroconversion rates in seronegative panels were 8.5% for flaviviruses and 24.2% for RR virus, and are broadly consistent with the cross-sectional study. CONCLUSIONS: Although flavivirus and alphavirus infections have occurred at a "steady rate"in western NSW and northern Victoria, there is a general lack of immunity to the agents of Australian encephalitis in all centres except Bourke. This needs to be considered in public health policy in these areas.

Adolescent↗
PubMed1999

[Present status of an arbovirus infection: yellow fever, its natural history of hemorrhagic fever, Rift Valley fever].

In the early 20th century, when it was discovered that the yellow fever virus was transmitted in its urban cycle by Aedes aegypti, measures of control were introduced leading to its disappearance. Progressive neglect of the disease, however, led to a new outbreak in 1927 during which the etiological agent was isolated; some years later a vaccine was discovered and yellow fever disappeared again. In the 1960s, rare cases of encephalitis were observed in young children after vaccination and the administration of the vaccine was forbidden for children under 10 years. Five years later, a new outbreak of yellow fever in Diourbel, Senegal, was linked to the presence of Aedes aegypti. In the late 1970s, the idea of a selvatic cycle for yellow fever arose. Thanks to new investigative techniques in Senegal and Côte d'Ivoire, the yellow fever virus was isolated from the reservoir of virus and vectors. The isolated virus was identified in monkeys and several vectors: Aedes furcifer, Aedes taylori, Aedes luteocephalus. Most importantly, the virus was isolated in male mosquitoes. Until recently, the only known cycle had been that of Haddow in East Africa. The virus circulate in the canopea between monkeys and Aedes africanus. These monkeys infect Aedes bromeliae when they come to eat in banana plantations. This cycle does not occur in West Africa. Vertical transmission is the main method of maintenance of the virus through the dry season. "Reservoirs of virus" are often mentioned in medical literature, monkeys having a short viremia whereas mosquitoes remain infected throughout their life cycle. In such a selvatic cycle, circulation can reach very high levels and no child would be able to escape an infecting bite and yet no clinical cases of yellow fever have been reported. The virulence--as it affects man--of the yellow fever virus in its wild cycle is very low. In areas where the virus can circulate in epidemic form, two types of circulation can be distinguished. Intermediate yellow fever--a term coined to define epidemia which do not correspond exactly to urban yellow fever. The cycle involves men and monkeys through wild vectors as Aedes furcifer but also through Aedes aegypti and the mortality rate is much lower than for urban epidemics. In urban yellow fever, man is the only vertebrate host involved in the circulation of the virus, the vector being generally Aedes aegypti. This vector maintains a selective pressure, increasing the transmission of virus capable of producing high viremia in man. In the selvatic cycles, two cycles can be distinguished: one of maintenance which does not increase the quantity of virus in circulation and one of amplification which does increase this quantity. As we shall see, it develops into an epizootic form but also in an epidemic form in man. When the decrease in yellow fevers across Africa is considered, it appears that all major epidemics occur in West Africa inspite of the presence of wild cycles of the yellow fever virus in Central and East Africa. For the rare epidemics that have occurred there, the vector has never been Aedes aegypti. In a recent outbreak in Kenya, the vector was Aedes bromeliae. The examination of part of the gene encoding for envelope protein showed the presence of two geographical types corresponding to West-Africa and Central East-Africa. Clinically speaking, yellow fever is an haemorrhagic fever with hepatitis similar to other haemorrhagic fevers such as Rift Valley fever. When, in 1987, an outbreak of haemorrhagic fever occurred in southern Mauritania, for several days it was thought to be yellow fever. Four days later, the diagnosis was corrected by isolating and identifying the virus as that of Rift Valley fever (RVFV). RVFV causes several pathogenic syndromes in human beings: acute febrile illness, haemorrhagic fever, haemorrhagic fever with hepatitis, nervous syndromes or ocular disease. Mortality rate was high for haemorrhagic fever with hepatitis, reaching 36%. (ABST

Aedes↗
PubMedDate not supplied

[Interferon production in vitro (by leukocytes) in response to arbovirus infections].

Experiments on cultivation of Semliki Forest virus in suspensions of the blood from immune and intact white mice and rabbits showed that adsorption of virus of phagocytosis by these cells occurred in the process of cultivation. There was a relationship between the rate of virus adsorption and interferon production: upon rapid virus adsorption by the immune cells interferon production by these cells was more intensive early after inoculation of the inducer. The dynamics of Semliki virus adsorption and of interferon production of leukocytes of white mice was close to that determined in cultivation of the virus in rabbit leukocyte suspension.

Adsorption↗
PubMed1975

Arbovirus infections in reptiles: studies on the presence of Japanese encephalitis virus antibody in the plasma of the turtle, Trionyx sinensis.

This study was undertaken to examine further the natural infection of poikilothermic animals e.g. turtles, to Japanese encephalitis (JE) virus. Plasma samples from 75 soft-shelled fresh water turtles (Trionyx sinensis Wiegman) from China were examined in virus neutralization (VN) and hemagglutination inhibition (HAI) tests for the presence of specific antibody. The total incidence of antibody detected by either test to a titer of 10 or greater was 89% while 77% and 60% were positive by VN and HAI tests, respectively. Forty-one per cent were jointly positive by both tests. Mean HAI and VN titers were similar and showed no obvious differences between spring/summer and autumn/winter seasons. The HAI reactivity was associated with a 7S component for both seasons. The significance of this inhibition in the serology of poikilothermic hosts and the possible behaviour of T. sinensis in the natural history of JE virus is briefly considered.

Animals↗
PubMedDate not supplied

Arbovirus infections of humans in New South Wales. Seroepidemiology of the flavivirus group of togaviruses.

A seroepidemiological study of 16 842 human sera, collected in 1981 and 1982 from all health regions of New South Wales, was carried out using the haemagglutination-inhibition (HI) test and eight Australasian flaviviruses: Murray Valley encephalitis (MVE); Kunjin (KUN); Alfuy (ALF); Stratford (STR); Kokobera (KOK); Edge Hill (EH); Sepik (SEP); and Saumarez Reef (SRE). A limited survey was also carried out with two recently discovered flaviviruses, Gadgets Gully and CSIRO 946. Antibody prevalence rates were low on the coast and tablelands (around 2%-8%), moderate on the western slopes (6%-11%) and high on the western plains (26%-42%). Some centres had higher prevalence rates, Bourke being the highest at 78%. The survey indicated that SEP and SRE viruses are unlikely to infect humans in New South Wales. Similarly, there was no evidence for Gadgets Gully and CSIRO 946 infection of humans. HI antibody prevalence rates were highest to STR, MVE, KUN and ALF in that order, these agents being closely related antigenetically. Reactions to KOK and EH occurred less frequently. Serological tests of greater specificity will be required to identify the flaviviruses that elicit these HI antibodies.

Adolescent↗
PubMed1984

Arbovirus infections in humans in New South Wales. Seroepidemiology of the alphavirus group of togaviruses.

A seroepidemiological study of the prevalence of antibodies to alphaviruses (Ross River [RRV], Sindbis [SIN] and Getah [GET] viruses) was carried out on 16 842 specimens of sera collected during 1981 and 1982 from individuals of all ages living in all health regions of New South Wales. Prevalence rates were found to be low in the major coastal cities of Sydney, Newcastle and Wollongong, and in the whole of the Tablelands. In coastal populations, the rates were highest in the far and mid North Coast zones (about 16%), and slightly lower in the south. The ratio of RRV:SIN antibodies was 62:1 in coastal populations. Antibody prevalence rates varied from 10%-20% in the Western Slopes, rising to 30%-40% in centres in the Western Plains; the RRV:SIN antibody ratio here was 11:1. The unexpectedly high infection rates, especially in the Western Plains, suggest that Ross River virus, in particular, may constitute a public health problem of hitherto unsuspected significance in New South Wales.

Adolescent↗