RESUMO
Human respiratory syncytial virus (RSV) is an important cause of acute respiratory infection (ARI) with the most severe disease in the young and elderly1,2. Non-pharmaceutical interventions (NPIs) and travel restrictions for controlling COVID-19 have impacted the circulation of most respiratory viruses including RSV globally, particularly in Australia, where during 2020 the normal winter epidemics were notably absent3-6. However, in late 2020, unprecedented widespread RSV outbreaks occurred, beginning in spring, and extending into summer across two widely separated states of Australia, Western Australia (WA) and New South Wales (NSW) including the Australian Capital Territory (ACT). Genome sequencing revealed a significant reduction in RSV genetic diversity following COVID-19 emergence except for two genetically distinct RSV-A clades. These clades circulated cryptically, likely localized for several months prior to an epidemic surge in cases upon relaxation of COVID-19 control measures. The NSW/ACT clade subsequently spread to the neighbouring state of Victoria (VIC) and caused extensive outbreaks and hospitalisations in early 2021. These findings highlight the need for continued surveillance and sequencing of RSV and other respiratory viruses during and after the COVID-19 pandemic as mitigation measures introduced may result in unusual seasonality, along with larger or more severe outbreaks in the future.
RESUMO
In the winter of 2003 Western Australia experienced its largest epidemic of influenza for at least five years, with activity peaking in August and September. The season was short resulting in very high numbers of cases during the peak weeks. Activity in country areas followed the peak of Metropolitan activity. Influenza A virus was detected in 28.3 per cent of the sentinel samples, and influenza B in less than one per cent. Both routine and sentinel detections and the overall estimates of influenza-like illnesses (ILI) seen by general practitioners at sentinel practices peaked in August and September 2003. The combination of influenza detections and an increase in ILI seemed to be the most accurate predictor of the beginning of winter influenza activity. There was a shift in age distribution for influenza A compared with 2003. Both the sentinel surveillance and routine samples demonstrated an increase of influenza in children and young adults. The majority of influenza A isolates were identified as A/Fujian/411/2002-like, a variant of the A/Moscow strain included in the vaccine. Despite this mismatch there did not seem to have been any noticeable increase in the risk of influenza infection in the vaccinated populations from the sentinel practices, nor was there a relative increase in disease among the highly vaccinated elderly population. A number of other respiratory viruses were identified as causes of influenza-like illness in the sentinel samples. Rhinoviruses and human metapneumovirus were the most common, the latter occurring mainly in adults.
