Zika virus and its potential re-emergence in Malaysia

Zika virus (ZIKV) has re-emerged to cause explosive epidemics in the Pacific and Latin America, and appears to be associated with severe neurological complications including microcephaly in babies. ZIKV is transmitted to humans by Aedes mosquitoes, principally Ae. aegypti, and there is historical evidence of ZIKV circulation in Southeast Asia. It is therefore clear that Malaysia is at risk of similar outbreaks. Local and international guidelines are available for surveillance, diagnostics, and management of exposed and infected individuals. ZIKV is the latest arbovirus to have spread globally beyond its initial restricted niche, and is unlikely to be the last. Innovative new methods for surveillance and control of vectors are needed to target mosquito-borne diseases as a whole.

Enterovirus 71 in Malaysia: A decade later

In the last decade, Malaysia has experienced several hand, foot and mouth disease (HFMD) epidemics, complicated by fatalities due to severe neurological involvement. Enterovirus 71 (EV-71) has been implicated as the major causative agent for these epidemics. EV-71 infection is a global public health problem with pandemic potential. In many parts of Asia-Pacifi c, the virus has emerged as one of the most deadly virus infections amongst young children. The virus is highly transmissible through faecaloral route and respiratory droplets. A recent rise in neurological complications and deaths suggests that the viruses currently circulating may be more virulent. The major risk factor associated with more severe EV-71 infection is young age and poor cellular immunity. Rapid laboratory diagnosis and molecular surveillance is important to closely monitor the emergence of new EV-71 subgenotypes. Since vaccine and anti-virals for EV-71 are not available, control and prevention strategies remain the only ways to combat the infection.

Enterovirus 71 infection induces apoptosis in Vero cells

The effects of Enterovirus 71 (HEV71) infection on African green monkey kidney cells (Vero) were investigated. It was found that the infected cells showed progressive cellular morphological changes characteristic in apoptotic cells within 10 hours post-infection. The number of apoptotic cells correlated significantly with the number of HEV71 antigen positive cells when cells were labeled using terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL) and stained for HEV71 antigen. Approximately 11, 26, 45 and 50% of the infected cells were apoptotic at 12, 24, 48 and 72 hours post-infection, respectively. Internucleosomal DNA fragmentation, characteristic in the late stage of apoptosis was noted beginning on day 2 post-infection. The DNA fragmentation, however, was absent in cells treated with the heat- and ultraviolet light-inactivated virus inocula. These results demonstrate the capacity of HEV71 to induce apoptosis in the infected cells. The induction, however, requires high level of HEV71 infectivity and the presence of live virus particles, suggesting the need for the presence of specific viral proteins for apoptosis to occur.