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  1. Chua KB, Lam SK, Sazaly AB, Lim ST, Paranjothy M
    Med J Malaysia, 1999 Mar;54(1):32-6.
    PMID: 10972002
    A provisional clinical diagnosis of exanthem subitum was made in six febrile infants seen in the Paediatric Unit of Assunta Hospital, Petaling Jaya, Malaysia with uvulo-palatoglossal junctional ulcers prior to the eruption of maculopapular rash. On follow-up, all six infants developed maculopapular rash with the subsidence of fever at the end of the fourth febrile day. Human herpesvirus 6 was isolated from the peripheral blood mononuclear cells during the acute phase of the illness and HHV 6 specific genome was also detected in these cells by nested polymerase chain reaction. All the six infants showed seroconversion for both specific IgG and IgM to the isolated virus. This study suggests that the presence of uvulo-palatoglossal junctional ulcers could be a useful early clinical sign of exanthem subitum due to human herpesvirus 6.
  2. Zawani MK, Abu HA, Sazaly AB, Zary SY, Darlina MN
    Genet. Mol. Res., 2014;13(4):8184-96.
    PMID: 25299203 DOI: 10.4238/2014.October.7.13
    The mosquito Aedes albopictus is indigenous to Southeast Asian and is a vector for arbovirus diseases. Studies examining the population genetics structure of A. albopictus have been conducted worldwide; however, there are no documented reports on the population genetic structure of A. albopictus in Malaysia, particularly in Penang. We examined the population genetics of A. albopictus based on a 445-base pair segment of the mitochondrial DNA cytochrome oxidase 1 gene among 77 individuals from 9 localities representing 4 regions (Seberang Perai Utara, Seberang Perai Tengah, Northeast, and Southwest) of Penang. A total of 37 haplotypes were detected, including 28 unique haplotypes. The other 9 haplotypes were shared among various populations. These shared haplotypes reflect the weak population genetic structure of A. albopictus. The phylogenetic tree showed a low bootstrap value with no genetic structure, which was supported by minimum spanning network analysis. Analysis of mismatch distribution showed poor fit of equilibrium distribution. The genetic distance showed low genetic variation, while pairwise FST values showed no significant difference between all regions in Penang except for some localities. High haplotype diversity and low nucleotide diversity was observed for cytochrome oxidase 1 mtDNA. We conclude that there is no population genetic structure of A. albopictus mosquitoes in the Penang area.
  3. Hassandarvish P, Tiong V, Sazaly AB, Mohamed NA, Arumugam H, Ananthanarayanan A, et al.
    Br Dent J, 2020 06;228(12):900.
    PMID: 32591671 DOI: 10.1038/s41415-020-1794-1
  4. Hoh BP, Umi-Shakina H, Zuraihan Z, Zaiharina MZ, Rafidah-Hanim S, Mahiran M, et al.
    Hum Immunol, 2015 Jun;76(6):421-6.
    PMID: 25858769 DOI: 10.1016/j.humimm.2015.03.019
    Dengue causes significantly more human disease than any other arboviruses. It causes a spectrum of illness, ranging from mild self-limited fever, to severe and fatal dengue hemorrhagic fever, as evidenced by vascular leakage and multifactorial hemostatic abnormalities. There is no specific treatment available till date. Evidence shows that chemokines CXCL10, CXCL11 and their receptor CXCR3 are involved in severity of dengue, but their genetic association with the susceptibility of vascular leakage during dengue infection has not been reported. We genotyped 14 common variants of these candidate genes in 176 patients infected with dengue. rs4859584 and rs8878 (CXCL10) were significantly associated with vascular permeability of dengue infection (P<0.05); while variants of CXCL11 showed moderate significance of association (P=0.0527). Haplotype blocks were constructed for genes CXCL10 and CXCL11 (5 and 7 common variants respectively). Haplotype association tests performed revealed that, "CCCCA" of gene CXCL10 and "AGTTTAC" of CXCL11 were found to be significantly associated with vascular leakage (P=0.0154 and 0.0366 respectively). In summary, our association study further strengthens the evidence of the involvement of CXCL10 and CXCL11 in the pathogenesis of dengue infection.
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