Volume 197 - Issue 3

Opportunistic serological surveillance for Murray Valley encephalitis virus in Victoria, February–May 2011

Authors:  Joseph S Doyle, Suellen Nicholson, Jennifer A Leydon, Rodney J Moran and Michael G Catton

Med J Aust 2012; 197 (3): 150. || doi: 10.5694/mja12.10221
Published online: 6 August 2012
To the Editor: Murray Valley encephalitis virus (MVEV) is rarely seen in south-eastern Australia, as described in the recent review in the Journal by Knox and colleagues.1 During the MVEV transmission period in early 2011, there was extensive flooding, and high notification rates were reported for other mosquito-transmitted infections, including flavivirus infection among horses. MVEV seroconversion was detected in sentinel chicken flocks. However, despite concerns ...

To the Editor: Murray Valley encephalitis virus (MVEV) is rarely seen in south-eastern Australia, as described in the recent review in the Journal by Knox and colleagues.1 During the MVEV transmission period in early 2011, there was extensive flooding, and high notification rates were reported for other mosquito-transmitted infections, including flavivirus infection among horses. MVEV seroconversion was detected in sentinel chicken flocks. However, despite concerns about widespread human disease, there were only four notifications of confirmed cases during this time.2 We designed a study to detect and monitor asymptomatic human transmission of MVEV to aid public health decisions about mosquito control.

Real-time opportunistic serological surveillance was conducted on sera referred sequentially to the Victorian Infectious Diseases Reference Laboratory from the Murray River region for other tests from February 2011 to May 2011. The surveillance was based on postcode data, and was conducted with approval from the Victorian Department of Health. An epitope-blocking ELISA (enzyme-linked immunosorbent assay) was performed to detect antibodies to MVEV or Kunjin virus (KUNV) in the samples. The results were compared with a reference sample matched by age and sex, obtained from metropolitan Melbourne. The monoclonal antibody assay was targeted against epitopes on the non-structural proteins NS1-10C6 (for MVEV) and 3.1112G (for KUNV), and results were considered positive if the monoclonal antibody inhibited binding by at least 50%.3,4

Overall, 346 samples (50% from males) were tested, with 65–73 individual samples from each month (total test sera, 268) compared with 78 baseline control sera. One hundred and thirteen individuals (42%) were born after the last regional outbreak of MVEV in 1974. MVEV antibodies were detected in 3.0% of samples overall (95% CI, 1.3%–5.8%). No individuals born after 1974 had detectable MVEV antibodies (95% CI, 0%–3.2%) (Box). The proportion of sera with detectable MVEV antibodies did not increase over time (Fisher exact test, P = 0.5). KUNV antibodies were detected in 2.2% of all samples (95% CI, 0.8%–4.8%), with no change over time, and no control sera had detectable antibodies to MVEV or KUNV (95% CI, 0%–4.6%).

Despite the environmental conditions in 2011 being favourable to MVEV spread, as predicted by the hypotheses of Forbes5 and Nicholls,6 MVEV seroprevalence was comparable to background rates.7 There was no serological evidence of recent human MVEV infection in this small, opportunistic sample, but low levels of infection may have been missed. Further study of the conditions in 2011 and close monitoring of MVEV activity in the future are needed to improve our understanding of human MVEV transmission.


Authors


Competing interests


References