The 2009 pandemic influenza A(H1N1) infection in Malaysia was first reported in May 2009 and oseltamivir was advocated for confirmed cases in postexposure prophylaxis. However, there are cases of oseltamivir-resistance reported among H1N1-positive patients in other countries. Resistance is due to substitution of histidine by tyrosine at residue 275 (H275Y) of neuraminidase (NA). In this study, we have employed Sanger sequencing method to investigate the occurrence of mutations in NA segments of 67 pandemic 2009 A(H1N1) viral isolates from Malaysian patients that could lead to probable oseltamivir resistance. The sequencing analysis did not yield mutation at residue 275 for all 67 isolates indicating that our viral isolates belong to the wild type and do not confer resistance to oseltamivir.
In March 2011, an outbreak of acute respiratory disease was reported at the Kuala Lumpur (Malaysia) Police Training Centre. Approximately 100 trainees were hospitalized and 5 were admitted to the intensive care unit. Three of these 5 trainees died. Human adenovirus type 7 was identified as the etiologic agent.
From 2005 to 2009, the Institute for Medical Research (IMR), Kuala Lumpur received a total of 7,117 respiratory specimens from patients with influenza-like illness (ILI) for influenza screening. Seasonal influenza virus was isolated from 17.3% of patients with ILI in 2005, 31.6% in 2006, 12.8% in 2007, 10.2% in 2008 and 13.5% in 2009. There were one or more influenza A and B virus strains circulating in Malaysia throughout the year, with distinctly a peak in May to August. The predominant circulating strains of seasonal influenza A were A/California/7/2004-like (H3N2) in 2005, A/New Caledonia/20/99-like (H1N1) in 2006, A/ Brisbane/10/2007-like (H3N2) in 2007 and 2008, and A/Perth/16/2009-like (H3N2) virus in 2009. The predominant circulating strains of influenza B were B/Hong Kong/330/2001-like in 2005, B/Malaysia/2506/2004-like in 2006, B/Florida/4/2006-like in 2007 and 2008, and B/Brisbane/60/2008-like in 2009.