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1 ant viruses, including chikungunya virus and Ross River virus.
2 used by other arthritogenic viruses, such as Ross River virus.
3 the E2 ectodomain in both Sindbis virus and Ross River virus.
4 itogenic alphaviruses, chikungunya virus and Ross River virus.
5 the distantly related dual-host alphavirus, Ross River virus.
6 assembled core particles of both Sindbis and Ross River viruses.
7 rions and compare their structure to that of Ross River virus, a togavirus belonging the genus Alphav
8 n this study, we show that two alphaviruses, Ross River virus and Chikungunya virus, lack the conserv
9 id protein gene from a different alphavirus, Ross River virus, and the second was to make deletions i
10 cluding Sindbis virus, Semliki Forest virus, Ross River virus, and Venezuelan equine encephalitis vir
13 ted with a related arthritogenic alphavirus, Ross River virus, but not in mice infected with West Nil
14 espite their similarities, Sindbis virus and Ross River virus capsid proteins do not form mixed core-
16 anged the length and/or charge of the NTD of Ross River virus CP and found that changing the charge o
18 ave isolated in both Sindbis virus E2 and in Ross River virus E1 a series of suppressing mutations th
19 uring passage of a chimeric virus containing Ross River virus E1 and Sindbis virus E2, the E2 change
21 of Sindbis virus are replaced with those of Ross River virus grow very poorly, but upon passage, ada
23 e nucleocapsid proteins of Sindbis virus and Ross River virus have been produced in a T7-based Escher
24 this modification expands the host range of Ross River virus in cultured cells to cells of avian ori
26 s using mammalian- and mosquito cell-derived Ross River virus (mam-RRV and mos-RRV, respectively) ind
27 with previous results, mosquito-cell-derived Ross River virus (mos-RRV) and Venezuelan equine encepha
28 Replication in both BHK and avian cells of Ross River virus mutants N218K and N218R was inhibited b
30 and polyprotein cleavage between Sindbis and Ross River virus mutants, despite the mutations being ma
31 iruses, including the Sindbis-group viruses, Ross River virus, O'nyong-nyong virus, and Chikungunya v
33 the 6K gene had been replaced with that from Ross River virus (RR) produced wild-type levels of nucle
34 tions in E2 of Sindbis virus (SIN) and E1 of Ross River virus (RR) that allow these two glycoproteins
38 orporate the glycoproteins of the alphavirus Ross River virus (RRV) and utilize them for entry into c
43 ther the vesicular stomatitis virus (VSV) or Ross River virus (RRV) envelope surface glycoproteins.
47 that contain the structural protein genes of Ross River virus (RRV) to investigate the location of th
48 explored vertebrate diversity and potential Ross River virus (RRV) transmission pathways by analysin
49 alphaviruses, chikungunya virus (CHIKV) and Ross River virus (RRV), and assessed the early antiviral
50 RTANCE Arthritogenic alphaviruses, including Ross River virus (RRV), are human pathogens that cause d
55 ses, including chikungunya virus (CHIKV) and Ross River virus (RRV), pose significant public health t
58 f the PE2 coding region of the T48 strain of Ross River virus (RRV-T48) with that from the attenuated
61 ing Sindbis virus nonstructural proteins and Ross River virus structural proteins growing considerabl
62 rity between these Sindbis virus mutants and Ross River virus suggests that E3 may also be present in
63 l form a heterodimer with glycoprotein E1 of Ross River virus that is cleaved to an E2/E1 heterodimer
64 imensions similar to that of the icosahedral Ross River virus, the present results indicate that rube
65 Cell surface binding of another alphavirus, Ross River virus, was found to be independent of heparan