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1 HTNV causes the most severe form of HFRS (5 to 15% case-
2 HTNV Gn is structurally conserved with the Gn of a genet
3 HTNV-infected cells treated with ribavirin showed a slig
7 ed trend for the peptides to inhibit SNV and HTNV to a greater extent than they inhibited PHV, a find
8 ng that supports the contention that SNV and HTNV use beta(3) integrins and PHV uses a different rece
9 novel peptides that inhibit entry by SNV and HTNV via beta(3) integrins and that can be used as lead
10 e were able to detect an interaction between HTNV N protein and importin alpha, a nuclear import mole
13 induce most cellular chemokines directed by HTNV (3/14) or genes primarily activated by NF-kappaB.
15 staining demonstrated that cells expressing HTNV N protein and a green fluorescent protein-p65 fusio
16 N protein showed an enhanced specificity for HTNV vRNA as compared with the S segment open reading fr
18 ER-Golgi intermediate compartment (ERGIC) in HTNV-infected Vero E6 cells, not with the ER, Golgi comp
20 ssociated elevation in mutation frequency in HTNV vRNA similar to that previously reported in vitro.
21 virin-treated mice, the amount of infectious HTNV was significantly decreased relative to that in unt
23 alyses demonstrated geographic clustering of HTNV strains from clinical specimens with the HTNV strai
27 rt here that the nucleocapsid (N) protein of HTNV was able to inhibit TNF-alpha-induced activation of
28 Here, we describe the crystal structure of HTNV envelope glycoprotein Gn, an integral component of
29 terize the inhibitory effect of ribavirin on HTNV, the levels of viral RNAs, proteins, and infectious
32 or sphingosine-1-phosphate (S1P) to ANDV- or HTNV-infected cells blocked VE-cadherin internalization
34 on of rhesus monkeys with either the SEOV or HTNV M gene elicited high levels of neutralizing antibod
35 , the assembly of Sin Nombre virus N protein-HTNV vRNA complexes was inhibited by the presence of Mg(
38 ein was examined for its ability to bind the HTNV S segment vRNA with filter binding and gel electrop
39 specific recognition of the HTNV vRNA by the HTNV N protein resides in the noncoding regions of the H
40 95-217 retained 94% of the vRNA bound by the HTNV N protein, while peptides 175-186 and 205-217 bound
44 a model in which specific recognition of the HTNV vRNA by the HTNV N protein resides in the noncoding
46 cells transfected with cDNA representing the HTNV N gene, were confirmed using HTNV-infected cells.
47 Structural overlay analysis reveals that the HTNV Gn fold is highly similar to the Gn of Puumala viru
49 TNV strains from clinical specimens with the HTNV strains circulating in rodents, suggesting the most
50 e studies mapped a minimal region within the HTNV N protein (amino acids 175 to 217) that bound vRNA.
51 d a positive selection for codons within the HTNV N protein gene in the ribavirin-treated vRNA popula
53 RNA increased to that observed for untreated HTNV-infected cells on day 2, whereas mRNA levels were m
54 contrast, the vRNA population in untreated, HTNV-infected mice showed a lower level of diversity, re
58 tivity and GTP repression for Hantaan virus (HTNV) and evidence for RBV's ability to promote error-pr
59 ogenic Andes virus (ANDV) and Hantaan virus (HTNV) and nonpathogenic Tula virus (TULV) hantaviruses.
60 virus (ANDV) and HFRS causing Hantaan virus (HTNV) are inhibited by alpha(v)beta(3) integrin antibodi
61 her whole genome sequences of Hantaan virus (HTNV) from HFRS patients and rodent hosts in endemic are
62 ), for the interaction of the Hantaan virus (HTNV) N protein and its genomic S segment (vRNA) was mea
63 acids 175 to 217) within the Hantaan virus (HTNV) N protein that interacts with a high affinity with
64 define the domain within the Hantaan virus (HTNV) N protein that mediates these interactions, 14 N-
67 ogenic NY-1 virus (NY-1V) and Hantaan virus (HTNV), nonpathogenic Prospect Hill virus (PHV) elicits e
71 e that Andes virus (ANDV)- or Hantaan virus (HTNV)-infected endothelial cells specifically direct the
72 n acts as a lethal mutagen in Hantaan virus (HTNV)-infected Vero E6 cells, resulting in an increased
75 [New York-1 virus (NY-1V) and Hantaan virus (HTNV)] bind immobilized beta3 polypeptides containing th
76 York-1 virus (NY-1V)], HFRS [Hantaan virus (HTNV)], or by a hantavirus not associated with human dis
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