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VP2 Exchange and NS3/NS3a Deletion in African Horse Sickness Virus (AHSV) in Development of Disabled Infectious Single Animal Vaccine Candidates for AHSV.

van de Water SG, van Gennip RG, Potgieter CA, Wright IM, van Rijn PA - J. Virol. (2015)

Bottom Line: Single Seg-2 AHSV reassortants showed similar cytopathogenic effects in mammalian cells but displayed different growth kinetics.Reverse genetics for AHSV was also used to study Seg-10 expressing NS3/NS3a proteins.African horse sickness has become a serious threat for countries outside Africa, since endemic Culicoides species in moderate climates are supposed to be competent vectors.

View Article: PubMed Central - PubMed

Affiliation: Department of Virology, Central Veterinary Institute of Wageningen UR (CVI), Lelystad, The Netherlands.

No MeSH data available.


Related in: MedlinePlus

Virus release form mammalian and insect cells. Monolayers were infected at an MOI of 0.1. Virus titers (log10 TCID50 per milliliter) in cell medium and cell fractions were determined at the indicated hours postinfection. (A) BSR cell-associated virus; (B) virus released from BSR cells; (C) KC-associated virus; (D) virus released from KC.
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Figure 4: Virus release form mammalian and insect cells. Monolayers were infected at an MOI of 0.1. Virus titers (log10 TCID50 per milliliter) in cell medium and cell fractions were determined at the indicated hours postinfection. (A) BSR cell-associated virus; (B) virus released from BSR cells; (C) KC-associated virus; (D) virus released from KC.

Mentions: The same set of selected Seg-10 mutants of AHSV4LP (mutAUG1+2&STOPS, delLD, delTM2, and delLD&delTM1+2) was studied for virus release from mammalian (BSR) and insect (KC) cells (Fig. 4). The virus titers of AHSV mutants in culture medium (released virus) of BSR cells were ∼1.5- to 2.0-log10 TCID50/ml lower than that of AHSV4LP (Fig. 4B). This difference was observed at 24 hpi and remained similar at 48 and 72 hpi. These results suggest that virus release is delayed in the first round of infection due to the lack of NS3/NS3a expression. The virus titer of cell-associated virus was 6 to 7 log10 TCID50/ml for both AHSV4LP and mutants of AHSV4LP, which indicated that virus replication in BSR cells is not affected by Seg-10 mutations (Fig. 4A).


VP2 Exchange and NS3/NS3a Deletion in African Horse Sickness Virus (AHSV) in Development of Disabled Infectious Single Animal Vaccine Candidates for AHSV.

van de Water SG, van Gennip RG, Potgieter CA, Wright IM, van Rijn PA - J. Virol. (2015)

Virus release form mammalian and insect cells. Monolayers were infected at an MOI of 0.1. Virus titers (log10 TCID50 per milliliter) in cell medium and cell fractions were determined at the indicated hours postinfection. (A) BSR cell-associated virus; (B) virus released from BSR cells; (C) KC-associated virus; (D) virus released from KC.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4524073&req=5

Figure 4: Virus release form mammalian and insect cells. Monolayers were infected at an MOI of 0.1. Virus titers (log10 TCID50 per milliliter) in cell medium and cell fractions were determined at the indicated hours postinfection. (A) BSR cell-associated virus; (B) virus released from BSR cells; (C) KC-associated virus; (D) virus released from KC.
Mentions: The same set of selected Seg-10 mutants of AHSV4LP (mutAUG1+2&STOPS, delLD, delTM2, and delLD&delTM1+2) was studied for virus release from mammalian (BSR) and insect (KC) cells (Fig. 4). The virus titers of AHSV mutants in culture medium (released virus) of BSR cells were ∼1.5- to 2.0-log10 TCID50/ml lower than that of AHSV4LP (Fig. 4B). This difference was observed at 24 hpi and remained similar at 48 and 72 hpi. These results suggest that virus release is delayed in the first round of infection due to the lack of NS3/NS3a expression. The virus titer of cell-associated virus was 6 to 7 log10 TCID50/ml for both AHSV4LP and mutants of AHSV4LP, which indicated that virus replication in BSR cells is not affected by Seg-10 mutations (Fig. 4A).

Bottom Line: Single Seg-2 AHSV reassortants showed similar cytopathogenic effects in mammalian cells but displayed different growth kinetics.Reverse genetics for AHSV was also used to study Seg-10 expressing NS3/NS3a proteins.African horse sickness has become a serious threat for countries outside Africa, since endemic Culicoides species in moderate climates are supposed to be competent vectors.

View Article: PubMed Central - PubMed

Affiliation: Department of Virology, Central Veterinary Institute of Wageningen UR (CVI), Lelystad, The Netherlands.

No MeSH data available.


Related in: MedlinePlus