Recombinant human enterovirus 71 in hand, foot and mouth disease patients

Hand, foot and mouth disease (HFMD) is a common illness of infants and young children less than 10 years of age. It is characterized by fever, ulcers in the oral cavity, and rashes with blisters that appear on the palm and sole. The most common causal agents of HFMD are coxsackievirus A16 (CV-A16) and human enterovirus 71 (HEV71), but other enteroviruses, including CV-A5 and CV-A10, can also cause it

FCGR3B gene copy number variation and host susceptibility to vascular leakage in Dengue Hemorrhagic Fever / Hoh Boon Peng , Sazaly Abu Bakar and Rafidah Hanim Shueb

DENV causes significantly more human disease than any other abovirus. Annually, an estimated of 50-100 million cases of severe dengue require hospitalization in which 500,000 resulted in DHF/DSS, with more than 20,000 death worldwide (WHO DengueNet report, 2005). Hence, it has now been recognized as a major expanding public health problem of the country. Dengue viruses cause a spectrum of illness ranging from asymptomatic infection or mild febrile illness to severe and fatal hemorrhagic disease. While majority experience uncomplicated Dengue Fever (DF), Dengue Hemorrhagic Fever (DHF) can present with severe clinical manifestations including transient vascular permeability resulting in plasma leakage (WHO, 1997). No specific treatment is available to date. Previous studies suggested the involvement of the events in the peripheral blood in association with the DENV disease severity, such as dengue viral replication, cytokine expression, and cellular activation / proliferation and robust host inflammatory immune response (Rothman, 2004). Antibody-dependent enhancement of viral replication is the most widely accepted explanation for the association between DHF and pre-existing antibody. However, it remains considerable uncertainty as to how virus-host interaction triggers the inflammatory response resulting in plasma leakage, the hallmark of DHF/DSS. FcGRII has been reported to play a role in pathogenesis of severe dengue infections (Loke et al., 2002; Littaua et al., 1990). It functions to mediate antibody enhancement in vitro by binding to virus-IgG complexes. A fundamental to any discussion of DENV pathogenesis is the association of secondary infection with heterologous serotypes with DHF/DSS. Antibody Dependent Enhancement (ADE) model during secondary infections, postulates that DENV specific antibodies either cross reactive antibodies, can interact with DENV without neutralizing the virus, and thereby requires FcG receptors to mediate entry of antibody coated DENV into cells (Clyde et al., 2006; Coffey et al, 2009). Therefore, this proposed study investigated and to characterized the CNV of FcGRII gene among the DF and DHF patients. Though association of FcGRII gene SNP polymorphism with dengue has been reported earlier (Loke et al, 2002), none investigated the copy number of this gene and its association to the susceptibility of plasma leakage

Isolation and molecular identification of Nipah virus from pigs

Nipah viruses from pigs from a Malaysian 1998 out-break were isolated and sequenced. At least two different Nipah virus strains, including a previously unreported strain, were identified. The findings highlight the possibility that the Malaysia outbreaks had two origins of Nipah virus infections

A Comparison of Assays for Accurate Copy Number Measurement of the Low-Affinity Fc Gamma Receptor Genes FCGR3A and FCGR3B

The FCGR3 locus encoding the low affinity activating receptor FcγRIII, plays a vital role in immunity triggered by cellular effector and regulatory functions. Copy number of the genes FCGR3A and FCGR3B has previously been reported to affect susceptibility to several autoimmune diseases and chronic inflammatory conditions. However, such genetic association studies often yield inconsistent results; hence require assays that are robust with low error rate. We investigated the accuracy and efficiency in estimating FCGR3 CNV by comparing Sequenom MassARRAY and paralogue ratio test-restriction enzyme digest variant ratio (RT-REDVR). In addition, since many genetic association studies of FCGR3B CNV were carried out using real-time quantitative PCR, we have also included the evaluation of that method’s performance in estimating the multi-allelic CNV of FCGR3B. The qPCR assay exhibited a considerably broader distribution of signal intensity, potentially introducing error in estimation of copy number and higher false positive rates. Both Sequenom and PRT-REDVR showed lesser systematic bias, but Sequenom skewed towards copy number normal (CN = 2). The discrepancy between Sequenom and PRT-REDVR might be attributed either to batch effects noise in individual measurements. Our study suggests that PRT-REDVR is more robust and accurate in genotyping the CNV of FCGR3, but highlights the needs of multiple independent assays for extensive validation when performing a genetic association study with multi-allelic CNVs

Temubual secara langsung Profesor Dr Sazaly bin Abu Bakar, Pengarah Tropical Infectious Diseases Research & Education Centre (TIDREC) Universiti Malaya (UM) di saluran TV1 (CH101) & radio KL fm

Saluran: TV1 Tarikh: 15 Mac 2018 (Khamis); Masa: 8.30 pagi; Rancangan: Selamat Pagi Malaysia; Tajuk: Risiko Jangkitan MERS-CoV bagi Jemaah Umrah Ikuti temubual secara online melalui pautan https://myklik.rtm.gov.my/live/10149 ~~~~~ Radio: KL fm Tarikh: 15 Mac 2018 (Khamis); Masa: 2.00 petang; Rancangan: Skop; Tajuk: Penyakit MERS-CoV - Terbawa Pulang Tanpa Sengaja Ikuti temubual secara online melalui pautan https://myklik.rtm.gov.my/radio/3811

Characterization of dengue type 2 new guinea C virus infection in c6/36, vero and MRC-5 cells.

Dengue viruses have been shown to infect a wide variety of cell lines with different consequences. In this study, cellular responses to dengue virus type 2 New Guinea C strain (D2NGC) viral infection in mosquito gut (C6/36), African green monkey kidney (Vero) and human lung fibroblast (MRC-5) cells were investigated. Microscopic and immunostaining studies of infected cells showed different patterns of infection in each cell lines reflecting the different degrees of permissiveness to D2NGC infection. Using a terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining method, we showed that D2NGC virus induced apoptosis in the three cell lines studied. However, the levels of apoptotic cells in each cell lines varied suggesting that programmed cell death is dependent on the unique properties of each cell lines. Results obtained from this study imply that diverse mechanisms are employed in D2NGC infection in different cells. This information will contribute towards further understanding of the mechanisms of DEN virus infection