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Results: 5

1.
Fig 3

Fig 3. From: Identification of Virulence Determinants within the L Genomic Segment of the Pichinde Arenavirus.

Liver pathology of infected animals. Shown is representative H&E staining of livers from guinea pigs infected with rP2, rP18, N1906D/N1889D, and N1906D/N1889D/L1839V/T1808A mutants.

Lisa McLay, et al. J Virol. 2013 June;87(12):6635-6643.
2.
Fig 4

Fig 4. From: Identification of Virulence Determinants within the L Genomic Segment of the Pichinde Arenavirus.

Growth curves of recombinant single or combination point mutant viruses. Vero cells were infected with various mutant viruses at an MOI of 0.01, and virus titers at various time points were determined by plaque assay.

Lisa McLay, et al. J Virol. 2013 June;87(12):6635-6643.
3.
Fig 5

Fig 5. From: Identification of Virulence Determinants within the L Genomic Segment of the Pichinde Arenavirus.

Real time RT-PCR analysis of genome replication in Vero cells infected with recombinant viruses. Vero cells were infected at an MOI of 1 with virus, RNA was collected, and RT was performed with a primer specific for the 3′ end of the genomic S segment. Real-time RT-PCR was performed with primers specific to the NP gene, and values were normalized with values for GAPDH transcripts. *, P < 0.05; **, P < 0.01; ***, P < 0.001.

Lisa McLay, et al. J Virol. 2013 June;87(12):6635-6643.
4.
Fig 2

Fig 2. From: Identification of Virulence Determinants within the L Genomic Segment of the Pichinde Arenavirus.

Mortality and viremia levels at terminal point of guinea pigs infected with single or combination point mutant viruses. (A) Mortality of animals infected with single point mutant viruses. Numbers of infected animals: rP18, n = 45, and recombinant mutant viruses, n = 6. (B) Mortality of animals infected with combination point mutant viruses. Numbers of infected animals: rP18, n = 45, and recombinant mutant viruses, n = 6. (C) Viremia levels at terminal points (or end of experiment for recovered animals) of guinea pigs infected with single and combination point mutant viruses. Each data point represents one animal: rP18, n = 29; N1889D mutant, n = 5; all other mutants, n = 6. *, P < 0.05; **, P < 0.01; ***, P < 0.001.

Lisa McLay, et al. J Virol. 2013 June;87(12):6635-6643.
5.
Fig 1

Fig 1. From: Identification of Virulence Determinants within the L Genomic Segment of the Pichinde Arenavirus.

(A) Generation of recombinant P2/P18 L segment fragment swapping mutants. Based on available unique restriction enzyme sites, 3 fragment swapping mutants were generated, replacing a fragment of the P18 L segment with the corresponding sequence of the P2 genome. Sequence changes are highlighted in black, and changes that result in amino acid differences between the two strains are numbered. (B) Mortality of guinea pigs infected with L segment P2/P18 fragment swapping mutant recombinant viruses. The mortality rate was defined as the number of animals reaching terminal points (>30% weight loss compared to a nomogram or rectal temperature of <38°C in addition to a marked decrease in the weight of the animal) within the course of an 18-day infection. Numbers of infected animals are as follows: rP18, n = 45; rP2, n = 24; rS18L18(A2), n = 8; rS18L18(C2), n = 3; and rS18L18(D2), n = 8. (C) Viremia levels of guinea pigs infected with L segment P2/P18 fragment swapping mutant recombinant viruses. Serum samples collected at terminal points (TP) from animals infected with rS18L18(D2), rS18L18(C2), or rS18L18(A2) were analyzed by plaque assay to determine viral titers. Each data point represents one animal: rP18, n = 29; rP2, n = 12; rS18L18(A2), n = 3; rS18L18(C2), n = 3; and rS18L18(D2), n = 6. dpi, days postinfection. *, P < 0.05; **, P < 0.01; ***, P < 0.001.

Lisa McLay, et al. J Virol. 2013 June;87(12):6635-6643.

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