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Donald K Milton - One of the best experts on this subject based on the ideXlab platform.
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airborne influenza Virus detection with four aerosol samplers using molecular and Infectivity assays considerations for a new infectious Virus aerosol sampler
Indoor Air, 2009Co-Authors: Patricia Fabian, James J Mcdevitt, Eugene Andres Houseman, Donald K MiltonAbstract:As a first step in conducting studies of airborne influenza transmission, we compared the collection performance of an SKC Biosampler, a compact cascade impactor (CCI), Teflon filters, and gelatin filters by collecting aerosolized influenza Virus in a one-pass aerosol chamber. Influenza Virus Infectivity was determined using a fluorescent focus assay and influenza Virus nucleic acid (originating from viable and non-viable Viruses) was measured using quantitative PCR. The results showed that the SKC Biosampler recovered and preserved influenza Virus Infectivity much better than the other samplers – the CCI, Teflon, and gelatin filters recovered only 7–22% of infectious Viruses compared with the Biosampler. Total Virus collection was not significantly different among the SKC Biosampler, the gelatin, and Teflon filters, but was significantly lower in the CCI. Results from this study show that a new sampler is needed for Virus aerosol sampling, as commercially available samplers do not efficiently collect and conserve Virus Infectivity. Applications for a new sampler include studies of airborne disease transmission and bioterrorism monitoring. Design parameters for a new sampler include high collection efficiency for fine particles and liquid sampling media to preserve Infectivity.
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airborne influenza Virus detection with four aerosol samplers using molecular and Infectivity assays considerations for a new infectious Virus aerosol sampler
Indoor Air, 2009Co-Authors: Patricia Fabian, James J Mcdevitt, Eugene Andres Houseman, Donald K MiltonAbstract:As a first step in conducting studies of airborne influenza transmission, we compared the collection performance of an SKC Biosampler, a compact cascade impactor (CCI), Teflon filters, and gelatin filters by collecting aerosolized influenza Virus in a one-pass aerosol chamber. Influenza Virus Infectivity was determined using a fluorescent focus assay and influenza Virus nucleic acid (originating from viable and non-viable Viruses) was measured using quantitative PCR. The results showed that the SKC Biosampler recovered and preserved influenza Virus Infectivity much better than the other samplers - the CCI, Teflon, and gelatin filters recovered only 7-22% of infectious Viruses compared with the Biosampler. Total Virus collection was not significantly different among the SKC Biosampler, the gelatin, and Teflon filters, but was significantly lower in the CCI. Results from this study show that a new sampler is needed for Virus aerosol sampling, as commercially available samplers do not efficiently collect and conserve Virus Infectivity. Applications for a new sampler include studies of airborne disease transmission and bioterrorism monitoring. Design parameters for a new sampler include high collection efficiency for fine particles and liquid sampling media to preserve Infectivity. Practical Implications New air samplers are needed to study infectious airborne Viruses and learn about airborne disease transmission. As a first step in designing a new air sampler to collect influenza Virus we evaluated four commercial samplers and determined necessary design parameters for a new collector.
Alan D T Barrett - One of the best experts on this subject based on the ideXlab platform.
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Yellow Fever Virus Infectivity for Bolivian Aedes aegypti Mosquitoes
2014Co-Authors: John-paul Mutebi, Alan D T Barrett, Alberto Gianella, Amelia Travassos Da Rosa, Robert B. Tesh, Stephen HiggsAbstract:The absence of urban yellow fever Virus (YFV) in Bolivian cities has been attributed to the lack of competent urban mosquito vectors. Experiments with Aedes aegypti from Santa Cruz, Bolivia, demonstrated infection (100%), dissemination (20%), and transmission of a Bolivian YFV strain (CENETROP-322). Yellow fever Virus (YFV) may cause severe hemor-rhagic fever in humans. The Virus is transmitted between susceptible vertebrate hosts by infected mosqui-toes in the genera Aedes, Haemagogus, or Sabethes (1). In the Americas, YFV occurs in two transmission cycles. In the jungle/sylvatic cycle, the Virus is transmitted between susceptible monkeys, and possibly other vertebrates, by tree-hole–breeding mosquitoes (1). Jungle yellow fever (YF) cases occur when these infected vectors feed on sus-ceptible humans. In the urban cycle, YFV is transmitted to humans by Aedes aegypti mosquitoes (1). In 2003, a total of 226 cases of jungle YF were reported from South America to the Pan American Health Organization, and as of June 23, ongoing outbreaks in Bolivia, Brazil, Colombia, and Peru during 2004 have thus far resulted in 86 confirmed cases and 41 deaths (2). An Ae. aegypti eradication campaign initiated by the Pan American Sanitary Bureau in 1947 eliminated this species from most of Central and South America, and urban YF disappeared from the Americas in the 1940s. However, during the past 20 years, many countries aban-doned Ae. aegypti control measures, and this urban vector now reoccupies almost the entire area of its distribution preeradication (1). Ae. aegypti was eradicated from Bolivia during the 1960s and 1970s but reappeared in the city of Santa Cruz in 1980, and epidemics of dengue fever occurred during the 1980s and 1990s (3). In 1997 to 1998, six cases of YF were reported among Santa Cruz residents, and some were regarded as urban YF cases (3); despite a population>1 million, low vaccine immunization cover-age, and the presence of Ae. aegypti (3), no urban YF out-break occurred. Based on these observations, researchers have suggested that sylvan strains of YFV circulating in Bolivia may not be infective for Bolivian Ae. aegypti. This study examined that hypothesis and the Infectivity of a Bolivian strain of YFV for Bolivian Ae. aegypti
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characterization of dengue Virus complex specific neutralizing epitopes on envelope protein domain iii of dengue 2 Virus
Journal of Virology, 2008Co-Authors: Gregory D Gromowski, Nicholas D Barrett, Alan D T BarrettAbstract:The surface of the mature dengue Virus (DENV) particle is covered with 180 envelope (E) proteins arranged as homodimers that lie relatively flat on the virion surface. Each monomer consists of three domains (ED1, ED2, and ED3), of which ED3 contains the critical neutralization determinant(s). In this study, a large panel of DENV-2 recombinant ED3 mutant proteins was used to physically and biologically map the epitopes of five DENV complex-specific monoclonal antibodies (MAbs). All five MAbs recognized a single antigenic site that includes residues K310, I312, P332, L389, and W391. The DENV complex antigenic site was located on an upper lateral surface of ED3 that was distinct but overlapped with a previously described DENV-2 type-specific antigenic site on ED3. The DENV complex-specific MAbs required significantly higher occupancy levels of available ED3 binding sites on the virion, compared to DENV-2 type-specific MAbs, in order to neutralize Virus Infectivity. Additionally, there was a great deal of variability in the neutralization efficacy of the DENV complex-specific MAbs with representative strains of the four DENVs. Overall, the differences in physical binding and potency of neutralization observed between DENV complex- and type-specific MAbs in this study demonstrate the critical role of the DENV type-specific antibodies in the neutralization of Virus Infectivity.
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characterization of an antigenic site that contains a dominant type specific neutralization determinant on the envelope protein domain iii ed3 of dengue 2 Virus
Virology, 2007Co-Authors: Gregory D Gromowski, Alan D T BarrettAbstract:The surface of the mature dengue Virus (DENV) particle consists of 90 envelope (E) protein dimers that mediate both receptor binding and fusion. The E protein ectodomain can be divided into three structural domains designated ED1, ED2, and ED3, of which ED3 contains the critical and dominant Virus-specific neutralization sites. In this study the ED3 epitopes recognized by seven, murine, IgG1 DENV-2 type-specific, monoclonal antibodies (MAbs) were determined using site-directed mutagenesis of a recombinant DENV-2 ED3 (rED3) protein. A total of 41 single amino acid substitutions were introduced into the rED3 at 30 different surface accessible residues. The affinity of each MAb with the mutant rED3s was assessed by indirect ELISA and the results indicate that all seven MAbs recognize overlapping epitopes with residues K305 and P384 critical for binding. These residues are conserved among DENV-2 strains and cluster together on the upper lateral face of ED3. A linear relationship was observed between relative occupancy of ED3 on the virion by MAb and neutralization of the majority of Virus Infectivity (∼ 90%) for all seven MAbs. Depending on the MAb, it is predicted that between 10% and 50% relative occupancy of ED3 on the virion is necessary for Virus neutralization and for all seven MAbs occupancy levels approaching saturation were required for 100% neutralization of Virus Infectivity. Overall, the conserved antigenic site recognized by all seven MAbs is likely to be a dominant DENV-2 type-specific, neutralization determinant.
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characterization of an antigenic site that contains a dominant type specific neutralization determinant on the envelope protein domain iii ed3 of dengue 2 Virus
Virology, 2007Co-Authors: Gregory D Gromowski, Alan D T BarrettAbstract:The surface of the mature dengue Virus (DENV) particle consists of 90 envelope (E) protein dimers that mediate both receptor binding and fusion. The E protein ectodomain can be divided into three structural domains designated ED1, ED2, and ED3, of which ED3 contains the critical and dominant Virus-specific neutralization sites. In this study the ED3 epitopes recognized by seven, murine, IgG1 DENV-2 type-specific, monoclonal antibodies (MAbs) were determined using site-directed mutagenesis of a recombinant DENV-2 ED3 (rED3) protein. A total of 41 single amino acid substitutions were introduced into the rED3 at 30 different surface accessible residues. The affinity of each MAb with the mutant rED3s was assessed by indirect ELISA and the results indicate that all seven MAbs recognize overlapping epitopes with residues K305 and P384 critical for binding. These residues are conserved among DENV-2 strains and cluster together on the upper lateral face of ED3. A linear relationship was observed between relative occupancy of ED3 on the virion by MAb and neutralization of the majority of Virus Infectivity (∼ 90%) for all seven MAbs. Depending on the MAb, it is predicted that between 10% and 50% relative occupancy of ED3 on the virion is necessary for Virus neutralization and for all seven MAbs occupancy levels approaching saturation were required for 100% neutralization of Virus Infectivity. Overall, the conserved antigenic site recognized by all seven MAbs is likely to be a dominant DENV-2 type-specific, neutralization determinant.
Tao Wang - One of the best experts on this subject based on the ideXlab platform.
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evolutionary enhancement of zika Virus Infectivity in aedes aegypti mosquitoes
Nature, 2017Co-Authors: Yang Liu, Jianying Liu, Chao Shan, Kaixiao Nie, Rudian Zhang, Renli Zhang, Tao WangAbstract:A mutation that increases the secretion of Zika Virus non-structural protein 1 (NS1) in infected hosts enhances the ability of the Virus to infect its mosquito vector Aedes aegypti and might have contributed to the recent Zika epidemic. Several flaviViruses, such as dengue fever Virus and Zika Virus, are transmitted by mosquitos. Gong Cheng and colleagues have previously shown that the acquisition of flaviViruses by mosquitoes can be influenced by the flaviVirus non-structural protein 1 (NS1), which can be secreted into the serum of an infected host and acquired by the mosquitoes together with the Virus. Here, the authors show that such a mechanism also operates to enhance the acquisition of Zika Virus (ZIKV) infection by its mosquito vector A. aegypti. The authors identify a mutation in NS1 that enhances its secretion and hence serves to increase mosquito acquisition of the Virus. In a survey of NS1 proteins from Asian isolates of ZIKV, the authors also find that the mutation is observed in all isolates collected after 2013. The authors speculate that this mutation in NS1 may have contributed to the rapid spread of the recent epidemic. Zika Virus (ZIKV) remained obscure until the recent explosive outbreaks in French Polynesia (2013–2014) and South America (2015–2016)1,2,3. Phylogenetic studies have shown that ZIKV has evolved into African and Asian lineages. The Asian lineage of ZIKV was responsible for the recent epidemics in the Americas1,3. However, the underlying mechanisms through which ZIKV rapidly and explosively spread from Asia to the Americas are unclear. Non-structural protein 1 (NS1) facilitates flaviVirus acquisition by mosquitoes from an infected mammalian host and subsequently enhances viral prevalence in mosquitoes4. Here we show that NS1 antigenaemia determines ZIKV Infectivity in its mosquito vector Aedes aegypti, which acquires ZIKV via a blood meal. Clinical isolates from the most recent outbreak in the Americas were much more infectious in mosquitoes than the FSS13025 strain, which was isolated in Cambodia in 2010. Further analyses showed that these epidemic strains have higher NS1 antigenaemia than the FSS13025 strain because of an alanine-to-valine amino acid substitution at residue 188 in NS1. ZIKV Infectivity was enhanced by this amino acid substitution in the ZIKV FSS13025 strain in mosquitoes that acquired ZIKV from a viraemic C57BL/6 mouse deficient in type I and II interferon (IFN) receptors (AG6 mouse). Our results reveal that ZIKV evolved to acquire a spontaneous mutation in its NS1 protein, resulting in increased NS1 antigenaemia. Enhancement of NS1 antigenaemia in infected hosts promotes ZIKV Infectivity and prevalence in mosquitoes, which could have facilitated transmission during recent ZIKV epidemics.
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evolutionary enhancement of zika Virus Infectivity in aedes aegypti mosquitoes
Nature, 2017Co-Authors: Senyan Du, Chao Shan, Rudian Zhang, Renli Zhang, Tao Wang, Xiaofeng Li, Penghua Wang, Gong ChengAbstract:A mutation that increases the secretion of Zika Virus non-structural protein 1 (NS1) in infected hosts enhances the ability of the Virus to infect its mosquito vector Aedes aegypti and might have contributed to the recent Zika epidemic. Several flaviViruses, such as dengue fever Virus and Zika Virus, are transmitted by mosquitos. Gong Cheng and colleagues have previously shown that the acquisition of flaviViruses by mosquitoes can be influenced by the flaviVirus non-structural protein 1 (NS1), which can be secreted into the serum of an infected host and acquired by the mosquitoes together with the Virus. Here, the authors show that such a mechanism also operates to enhance the acquisition of Zika Virus (ZIKV) infection by its mosquito vector A. aegypti. The authors identify a mutation in NS1 that enhances its secretion and hence serves to increase mosquito acquisition of the Virus. In a survey of NS1 proteins from Asian isolates of ZIKV, the authors also find that the mutation is observed in all isolates collected after 2013. The authors speculate that this mutation in NS1 may have contributed to the rapid spread of the recent epidemic. Zika Virus (ZIKV) remained obscure until the recent explosive outbreaks in French Polynesia (2013–2014) and South America (2015–2016)1,2,3. Phylogenetic studies have shown that ZIKV has evolved into African and Asian lineages. The Asian lineage of ZIKV was responsible for the recent epidemics in the Americas1,3. However, the underlying mechanisms through which ZIKV rapidly and explosively spread from Asia to the Americas are unclear. Non-structural protein 1 (NS1) facilitates flaviVirus acquisition by mosquitoes from an infected mammalian host and subsequently enhances viral prevalence in mosquitoes4. Here we show that NS1 antigenaemia determines ZIKV Infectivity in its mosquito vector Aedes aegypti, which acquires ZIKV via a blood meal. Clinical isolates from the most recent outbreak in the Americas were much more infectious in mosquitoes than the FSS13025 strain, which was isolated in Cambodia in 2010. Further analyses showed that these epidemic strains have higher NS1 antigenaemia than the FSS13025 strain because of an alanine-to-valine amino acid substitution at residue 188 in NS1. ZIKV Infectivity was enhanced by this amino acid substitution in the ZIKV FSS13025 strain in mosquitoes that acquired ZIKV from a viraemic C57BL/6 mouse deficient in type I and II interferon (IFN) receptors (AG6 mouse). Our results reveal that ZIKV evolved to acquire a spontaneous mutation in its NS1 protein, resulting in increased NS1 antigenaemia. Enhancement of NS1 antigenaemia in infected hosts promotes ZIKV Infectivity and prevalence in mosquitoes, which could have facilitated transmission during recent ZIKV epidemics.
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evolutionary enhancement of zika Virus Infectivity in aedes aegypti mosquitoes
Nature, 2017Co-Authors: Yang Liu, Jianying Liu, Chao Shan, Kaixiao Nie, Rudian Zhang, Renli Zhang, Tao WangAbstract:Zika Virus (ZIKV) remained obscure until the recent explosive outbreaks in French Polynesia (2013-2014) and South America (2015-2016). Phylogenetic studies have shown that ZIKV has evolved into African and Asian lineages. The Asian lineage of ZIKV was responsible for the recent epidemics in the Americas. However, the underlying mechanisms through which ZIKV rapidly and explosively spread from Asia to the Americas are unclear. Non-structural protein 1 (NS1) facilitates flaviVirus acquisition by mosquitoes from an infected mammalian host and subsequently enhances viral prevalence in mosquitoes. Here we show that NS1 antigenaemia determines ZIKV Infectivity in its mosquito vector Aedes aegypti, which acquires ZIKV via a blood meal. Clinical isolates from the most recent outbreak in the Americas were much more infectious in mosquitoes than the FSS13025 strain, which was isolated in Cambodia in 2010. Further analyses showed that these epidemic strains have higher NS1 antigenaemia than the FSS13025 strain because of an alanine-to-valine amino acid substitution at residue 188 in NS1. ZIKV Infectivity was enhanced by this amino acid substitution in the ZIKV FSS13025 strain in mosquitoes that acquired ZIKV from a viraemic C57BL/6 mouse deficient in type I and II interferon (IFN) receptors (AG6 mouse). Our results reveal that ZIKV evolved to acquire a spontaneous mutation in its NS1 protein, resulting in increased NS1 antigenaemia. Enhancement of NS1 antigenaemia in infected hosts promotes ZIKV Infectivity and prevalence in mosquitoes, which could have facilitated transmission during recent ZIKV epidemics.
Yang Liu - One of the best experts on this subject based on the ideXlab platform.
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evolutionary enhancement of zika Virus Infectivity in aedes aegypti mosquitoes
Nature, 2017Co-Authors: Yang Liu, Jianying Liu, Chao Shan, Kaixiao Nie, Rudian Zhang, Renli Zhang, Tao WangAbstract:A mutation that increases the secretion of Zika Virus non-structural protein 1 (NS1) in infected hosts enhances the ability of the Virus to infect its mosquito vector Aedes aegypti and might have contributed to the recent Zika epidemic. Several flaviViruses, such as dengue fever Virus and Zika Virus, are transmitted by mosquitos. Gong Cheng and colleagues have previously shown that the acquisition of flaviViruses by mosquitoes can be influenced by the flaviVirus non-structural protein 1 (NS1), which can be secreted into the serum of an infected host and acquired by the mosquitoes together with the Virus. Here, the authors show that such a mechanism also operates to enhance the acquisition of Zika Virus (ZIKV) infection by its mosquito vector A. aegypti. The authors identify a mutation in NS1 that enhances its secretion and hence serves to increase mosquito acquisition of the Virus. In a survey of NS1 proteins from Asian isolates of ZIKV, the authors also find that the mutation is observed in all isolates collected after 2013. The authors speculate that this mutation in NS1 may have contributed to the rapid spread of the recent epidemic. Zika Virus (ZIKV) remained obscure until the recent explosive outbreaks in French Polynesia (2013–2014) and South America (2015–2016)1,2,3. Phylogenetic studies have shown that ZIKV has evolved into African and Asian lineages. The Asian lineage of ZIKV was responsible for the recent epidemics in the Americas1,3. However, the underlying mechanisms through which ZIKV rapidly and explosively spread from Asia to the Americas are unclear. Non-structural protein 1 (NS1) facilitates flaviVirus acquisition by mosquitoes from an infected mammalian host and subsequently enhances viral prevalence in mosquitoes4. Here we show that NS1 antigenaemia determines ZIKV Infectivity in its mosquito vector Aedes aegypti, which acquires ZIKV via a blood meal. Clinical isolates from the most recent outbreak in the Americas were much more infectious in mosquitoes than the FSS13025 strain, which was isolated in Cambodia in 2010. Further analyses showed that these epidemic strains have higher NS1 antigenaemia than the FSS13025 strain because of an alanine-to-valine amino acid substitution at residue 188 in NS1. ZIKV Infectivity was enhanced by this amino acid substitution in the ZIKV FSS13025 strain in mosquitoes that acquired ZIKV from a viraemic C57BL/6 mouse deficient in type I and II interferon (IFN) receptors (AG6 mouse). Our results reveal that ZIKV evolved to acquire a spontaneous mutation in its NS1 protein, resulting in increased NS1 antigenaemia. Enhancement of NS1 antigenaemia in infected hosts promotes ZIKV Infectivity and prevalence in mosquitoes, which could have facilitated transmission during recent ZIKV epidemics.
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evolutionary enhancement of zika Virus Infectivity in aedes aegypti mosquitoes
Nature, 2017Co-Authors: Yang Liu, Jianying Liu, Chao Shan, Kaixiao Nie, Rudian Zhang, Renli Zhang, Tao WangAbstract:Zika Virus (ZIKV) remained obscure until the recent explosive outbreaks in French Polynesia (2013-2014) and South America (2015-2016). Phylogenetic studies have shown that ZIKV has evolved into African and Asian lineages. The Asian lineage of ZIKV was responsible for the recent epidemics in the Americas. However, the underlying mechanisms through which ZIKV rapidly and explosively spread from Asia to the Americas are unclear. Non-structural protein 1 (NS1) facilitates flaviVirus acquisition by mosquitoes from an infected mammalian host and subsequently enhances viral prevalence in mosquitoes. Here we show that NS1 antigenaemia determines ZIKV Infectivity in its mosquito vector Aedes aegypti, which acquires ZIKV via a blood meal. Clinical isolates from the most recent outbreak in the Americas were much more infectious in mosquitoes than the FSS13025 strain, which was isolated in Cambodia in 2010. Further analyses showed that these epidemic strains have higher NS1 antigenaemia than the FSS13025 strain because of an alanine-to-valine amino acid substitution at residue 188 in NS1. ZIKV Infectivity was enhanced by this amino acid substitution in the ZIKV FSS13025 strain in mosquitoes that acquired ZIKV from a viraemic C57BL/6 mouse deficient in type I and II interferon (IFN) receptors (AG6 mouse). Our results reveal that ZIKV evolved to acquire a spontaneous mutation in its NS1 protein, resulting in increased NS1 antigenaemia. Enhancement of NS1 antigenaemia in infected hosts promotes ZIKV Infectivity and prevalence in mosquitoes, which could have facilitated transmission during recent ZIKV epidemics.
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evolutionary enhancement of zika Virus Infectivity in aedes aegypti mosquitoes
Nature, 2017Co-Authors: Yang Liu, Jianying Liu, Chao Shan, Kaixiao Nie, Rudian Zhang, Senyan Du, Xiaofeng Li, Renli ZhangAbstract:A mutation that increases the secretion of Zika Virus non-structural protein 1 (NS1) in infected hosts enhances the ability of the Virus to infect its mosquito vector Aedes aegypti and might have contributed to the recent Zika epidemic.
Patricia Fabian - One of the best experts on this subject based on the ideXlab platform.
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airborne influenza Virus detection with four aerosol samplers using molecular and Infectivity assays considerations for a new infectious Virus aerosol sampler
Indoor Air, 2009Co-Authors: Patricia Fabian, James J Mcdevitt, Eugene Andres Houseman, Donald K MiltonAbstract:As a first step in conducting studies of airborne influenza transmission, we compared the collection performance of an SKC Biosampler, a compact cascade impactor (CCI), Teflon filters, and gelatin filters by collecting aerosolized influenza Virus in a one-pass aerosol chamber. Influenza Virus Infectivity was determined using a fluorescent focus assay and influenza Virus nucleic acid (originating from viable and non-viable Viruses) was measured using quantitative PCR. The results showed that the SKC Biosampler recovered and preserved influenza Virus Infectivity much better than the other samplers – the CCI, Teflon, and gelatin filters recovered only 7–22% of infectious Viruses compared with the Biosampler. Total Virus collection was not significantly different among the SKC Biosampler, the gelatin, and Teflon filters, but was significantly lower in the CCI. Results from this study show that a new sampler is needed for Virus aerosol sampling, as commercially available samplers do not efficiently collect and conserve Virus Infectivity. Applications for a new sampler include studies of airborne disease transmission and bioterrorism monitoring. Design parameters for a new sampler include high collection efficiency for fine particles and liquid sampling media to preserve Infectivity.
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airborne influenza Virus detection with four aerosol samplers using molecular and Infectivity assays considerations for a new infectious Virus aerosol sampler
Indoor Air, 2009Co-Authors: Patricia Fabian, James J Mcdevitt, Eugene Andres Houseman, Donald K MiltonAbstract:As a first step in conducting studies of airborne influenza transmission, we compared the collection performance of an SKC Biosampler, a compact cascade impactor (CCI), Teflon filters, and gelatin filters by collecting aerosolized influenza Virus in a one-pass aerosol chamber. Influenza Virus Infectivity was determined using a fluorescent focus assay and influenza Virus nucleic acid (originating from viable and non-viable Viruses) was measured using quantitative PCR. The results showed that the SKC Biosampler recovered and preserved influenza Virus Infectivity much better than the other samplers - the CCI, Teflon, and gelatin filters recovered only 7-22% of infectious Viruses compared with the Biosampler. Total Virus collection was not significantly different among the SKC Biosampler, the gelatin, and Teflon filters, but was significantly lower in the CCI. Results from this study show that a new sampler is needed for Virus aerosol sampling, as commercially available samplers do not efficiently collect and conserve Virus Infectivity. Applications for a new sampler include studies of airborne disease transmission and bioterrorism monitoring. Design parameters for a new sampler include high collection efficiency for fine particles and liquid sampling media to preserve Infectivity. Practical Implications New air samplers are needed to study infectious airborne Viruses and learn about airborne disease transmission. As a first step in designing a new air sampler to collect influenza Virus we evaluated four commercial samplers and determined necessary design parameters for a new collector.
