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박만성(Man Seong Park) 한국보건의료연구원 2016 근거와 가치 Vol.2 No.2
In the wake of a surge of cases of microcephaly and Guillain-Barre syndrome in Brazil, association of which with Zika virus infection has now been confirmed, the World Health Organization declared ‘Public Health Emergency of International Concern’. Once an obscure mosquito-borne virus due to mildness of the disease caused by the virus, Zika has become a virus that humanity must overcome with an all-out effort. In this article, we briefly review current knowledge of the virus, the vector, the epidemiological situation and the response strategy. In the context of general understanding of the virus and public health crisis, we highlight three papers that have been seminal in terms of confirming the apparent association of Zika virus infection and the neurological manifestations such as microcephaly and Guillain-Barre syndrome, and bringing attention to a possibility of a different way of the Zika infection-mediated neurological manifestation such as acute myelitis.
( Se Hee Park ),( Jin Il Kim ),( Ilseob Lee ),( Joon Yong Bae ),( Min Woong Hwang ),( Dong Hwan Kim ),( Seok Il Jang ),( Hye Jin Kim ),( Mee Sook Park ),( Young Ki Choi ),박만성 ( Man Seong Park ) 대한인수공통전염병학회 2014 창립총회 및 학술대회 초록집 Vol.2014 No.1
Since March 2013, avian influenza H7N9 virus has caused human infections with resulting in an estimated 30% case fatality rate. Although there has been no evidence of sustained human-to-human transmission, effective medical responses and preparedness should be implemented including developing vaccines. Using the hemagglutinin (HA) of A/Anhui/1/2013, a prototype virus recommended for the H7N9 vaccine development by the World Health Organization, we investigated the effects of HA glycosylation on the growth kinetics and immunogenicity of recombinant viruses that generated in the backbone of a 2009 pandemic H1N1 virus. Glycosylation at HA residue increased viral growths both in cultured cells and in fertile chicken eggs whereas deglycosylation at HA residue decreased them all. When HA glycosites were utilized together, the virus exhibited the greatest replication property. In the hemagglutinin inhibition assay using guinea pig antisera raised against each virus. These antisera showed 1.75- to 4-fold increased immunogenicity across all of the tested viruses. Considered all, these results suggest that specific HA mutation can increase potential of a H7N9 vaccine virus by enhancing growth and immune properties.
남아프리카 지역내 한타바이러스 존재에 관한 혈청 역학적 증거
이평우(Pyung Woo Lee),박만성(Man Seong Park),G. Anthony Keen,Z. Noveljic,Tim J. Tucker,Elna van der Ryst,Johannes I. Viljoen,Anne-Marie Pretorius,Mike Oelofsen 대한바이러스학회 1999 Journal of Bacteriology and Virology Vol.29 No.1
Sero-epidemiologic survey has been carried out to establish serologically the presence of hantavirus in areas of South Africa. The survey was oriented to search natural infection in both of humans and wild rodents and involvement of human disease. The normal human sera were collected from the residents in urban and rural areas of Western Cape, and rural area of Eastern Cape province. The rodent sera came from various species of rodents trapped in Northern Cape and Western Free provinces. The patient sera were selected from the patients of renal failure, pulmonary syndrome and pyrexia of unknown origin (PVO) according to diagnostic chart among the patients hospitalized in major hospitals of Cape Town area. The sera were screened and titrated by IFA test using antigens of Hantaan (HTN), Seoul (SEO), Puumala (PUU), and Prospect Hill (PH) viruses primarily. Positive cases were subjected to differential IFA test using HTN, PUU and PH antigens and plaque reduction neutralization test for further confirmation. Anti-hantavirus antibodies were detected from 2 of 352 rural, 1 of 172 urban residents of E. Cape, and 5 of 118 rural, 5 of 368 urban residents of W. Cape. The antibody was also demonstrated from 5 of 221 wild rodents, and it was appeared that 2 different species, Aethomys namaquensis and Tatera leucogaster, are involved. Among 318 patients tested, 3 who were diagnosed as chronic renal failure, acute respiratory distress syndrome (ARDS) and glomerulonephritis were proved to be positive. The reaction patterns obtained from all of these positive sera were distinct from hantaviral sero-patterns ever established. This result suggests that new viruses may exist in this area and play an possible etiologic role in human disease. The feature of serologic survey on anti-hantavirus antibody demonstrable newly from African wild rodents which are different from reservoir species in other continents elicits a conjecture that the virus may be different from known hantaviruses ever found. This fact also suggests that an expanded role in etiologic involvement with other unknown human diseases by newly emerging hantaviruses may be possible in this areas.
Session 1: 사람-동물간 접점에서 인플루엔자의 감시 및 관리 : 인플루엔자바이러스의 전파력 및 관여 요인
( Jin Il Kim ),( Ilseob Lee ),( Se Hee Park ),( Min Woong Hwang ),( Joon Yong Bae ),( Sang Moo Lee ),( Jun Heo ),( Mee Sook Park ),박만성 ( Man Seong Park ) 대한인수공통전염병학회 2013 창립총회 및 학술대회 초록집 Vol.2013 No.1
Among three types of seasonal influenza viruses (H1N1, H3N2, and B) in humans, H1N1 viruses caused two pandemics in 1918 and 2009. Based on structural and serological studies, 1918 and 2009 H1N1 viruses are known to be antigenically similar. In addition, both viruses share specific genetic signatures of their hemagglutinins (HA), including the same glycosylation status. Since 1918, the H1 HA had utilized varying combinations of glycosylation in defined sites most likely as a strategy to antigenically change and evade pre-existing immunity. By analyzing possible genetic signatures in the HA associated with its glycosylation, we found that in the absence of residue, HA proteins were never glycosylated at residues 144 and 172. Thus, we investigated whether specific residue compensates with potential loss of viral fitness associated with HA glycosylation using 2009 H1N1 mutant viruses. Our analysis demonstrate that changes at specific HA residue sustain viral fitness by buffering glycosylation impact on pathogenesis and transmissibility.