81 Studies on the mechanism by which mutations at His274 alter sensitivity of influenza A virus neuraminidase type 1 to GS4071 and zanamivir

2000 ◽  
Vol 46 (1) ◽  
pp. A60 ◽  
Diabetologia ◽  
2015 ◽  
Vol 58 (11) ◽  
pp. 2592-2595 ◽  
Author(s):  
Anita Kondrashova ◽  
Noora Nurminen ◽  
Maarit Patrikainen ◽  
Heini Huhtala ◽  
Jussi Lehtonen ◽  
...  

1986 ◽  
Vol 59 (2) ◽  
pp. 377-383 ◽  
Author(s):  
J D Parvin ◽  
A Moscona ◽  
W T Pan ◽  
J M Leider ◽  
P Palese

2019 ◽  
Vol 66 (2) ◽  
pp. 696-704
Author(s):  
Scott M. Reid ◽  
Ruth Manvell ◽  
James M. Seekings ◽  
Vanessa Ceeraz ◽  
Helen Errington ◽  
...  

2017 ◽  
Vol 113 ◽  
pp. 233-241 ◽  
Author(s):  
Caiyun Huo ◽  
Shouping Zhang ◽  
Siyi Zhang ◽  
Ming Wang ◽  
Peng Qi ◽  
...  

2001 ◽  
Vol 75 (19) ◽  
pp. 8899-8908 ◽  
Author(s):  
Boris Ferko ◽  
Jana Stasakova ◽  
Sabine Sereinig ◽  
Julia Romanova ◽  
Dietmar Katinger ◽  
...  

ABSTRACT We have generated recombinant influenza A viruses belonging to the H1N1 and H3N2 virus subtypes containing an insertion of the 137 C-terminal amino acid residues of the human immunodeficiency virus type 1 (HIV-1) Nef protein into the influenza A virus nonstructural-protein (NS1) reading frame. These viral vectors were found to be genetically stable and capable of growing efficiently in embryonated chicken eggs and tissue culture cells but did not replicate in the murine respiratory tract. Despite the hyperattenuated phenotype of influenza/NS-Nef viruses, a Nef and influenza virus (nucleoprotein)-specific CD8+-T-cell response was detected in spleens and the lymph nodes draining the respiratory tract after a single intranasal immunization of mice. Compared to the primary response, a marked enhancement of the CD8+-T-cell response was detected in the systemic and mucosal compartments, including mouse urogenital tracts, if mice were primed with the H1N1 subtype vector and subsequently boosted with the H3N2 subtype vector. In addition, Nef-specific serum IgG was detected in mice which were immunized twice with the recombinant H1N1 and then boosted with the recombinant H3N2 subtype virus. These findings may contribute to the development of alternative immunization strategies utilizing hyperattenuated live recombinant influenza virus vectors to prevent or control infectious diseases, e.g., HIV-1 infection.


1998 ◽  
Vol 9 (3) ◽  
pp. 233-243 ◽  
Author(s):  
C McGuigan ◽  
A Perry ◽  
CJ Yarnold ◽  
PW Sutton ◽  
D Lowe ◽  
...  

A number of symmetric and asymmetric 5′-phosphate esters of the potent anti-varicellazoster virus (VZV) agent 1–(β-d-arabinofuranosyl)-5-prop-1-ynyluracil (882C; netivudine) were prepared as potential lipophilic, membrane-soluble prodrugs of the bioactive phosphate forms. The compounds were prepared by the base-catalysed coupling of various phosphorochloridates with the free nucleoside analogue. Compounds were fully characterized by a range of spectroscopic and analytical methods and were studied for their inhibition of several viruses in tissue culture. All of the phosphate esters were inactive against human cytomegalovirus, herpes simplex virus type 2, VZV, human immunodeficiency virus type 1 and influenza A virus (EC50 >100 μM) except the 5′-(4–nitrophenyl phenyl) phosphate, which inhibited influenza A virus. The relative rate of esterase-mediated hydrolysis of one of the lead target structures was measured in order to rationalize the poor antiviral action, and data were collected on possible metabolites in support of this analysis. Cell-specific esterases are implicated as key determinants of the antiviral potency of prodrugs of this type.


2000 ◽  
Vol 74 (10) ◽  
pp. 4505-4511 ◽  
Author(s):  
Ligia A. Pinto ◽  
Vesna Blazevic ◽  
Bruce K. Patterson ◽  
C. Mac Trubey ◽  
Matthew J. Dolan ◽  
...  

ABSTRACT It is now recognized that, in addition to drug-mediated therapies against human immunodeficiency virus type 1 (HIV-1), the immune system can exert antiviral effects via CD8+ T-cell-generated anti-HIV factors. This study demonstrates that (i) supernatants from peripheral blood mononuclear cells (PBMC) stimulated with influenza A virus inhibit replication of CCR5- and CXCR4-tropic HIV-1 isolates prior to reverse transcription; (ii) the HIV-suppressive supernatants can be generated by CD4- or CD8-depleted PBMC; (iii) this anti-HIV activity is partially due to alpha interferon (IFN-α), but not to IFN-γ, IFN-β, the β-chemokines MIP-1α, MIP-1β, and RANTES, or interleukin-16; (iv) the anti-HIV activity is generated equally well by PBMC cultured with either infectious or UV-inactivated influenza A virus; and (v) the antiviral activity can be generated by influenza A-stimulated PBMC from HIV-infected individuals. These findings represent a novel mechanism for inhibition of HIV-1 replication that differs from the previously described CD8 anti-HIV factors (MIP-1α, MIP-1β, RANTES, and CD8 antiviral factor).


2005 ◽  
Vol 79 (19) ◽  
pp. 12132-12147 ◽  
Author(s):  
Xinzhen Yang ◽  
Svetla Kurteva ◽  
Xinping Ren ◽  
Sandra Lee ◽  
Joseph Sodroski

ABSTRACT The human immunodeficiency virus type 1 (HIV-1) envelope glycoproteins (Envs) function as a trimer, mediating virus entry by promoting the fusion of the viral and target cell membranes. HIV-1 Env trimers induce membrane fusion through a pH-independent pathway driven by the interaction between an Env trimer and its cellular receptors, CD4 and CCR5/CXCR4. We studied viruses with mixed heterotrimers of wild-type and dominant-negative Envs to determine the number (T) of Env trimers required for HIV-1 entry. To our surprise, we found that a single Env trimer is capable of supporting HIV-1 entry; i.e., T = 1. A similar approach was applied to investigate the entry stoichiometry of envelope glycoproteins from amphotropic murine leukemia virus (A-MLV), avian sarcoma/leukosis virus type A (ASLV-A), and influenza A virus. When pseudotyped on HIV-1 virions, the A-MLV and ASLV-A Envs also exhibit a T = 1 entry stoichiometry. In contrast, eight to nine influenza A virus hemagglutinin trimers function cooperatively to achieve membrane fusion and virus entry, using a pH-dependent pathway. The different entry requirements for cooperativity among Env trimers for retroviruses and influenza A virus may influence viral strategies for replication and evasion of the immune system.


2019 ◽  
Vol 476 (3) ◽  
pp. 467-481 ◽  
Author(s):  
Jian Li ◽  
Siqi Hu ◽  
Fengwen Xu ◽  
Shan Mei ◽  
Xiaoman Liu ◽  
...  

AbstractMOV10 has emerged as an important host antiviral factor. MOV10 not only inhibits various viruses, including human immunodeficiency virus type 1, hepatitis C virus and vesicular stomatitis virus, but also restricts the activity of retroelements long interspersed nucleotide element-1, Alu, SVA and intracisternal A particles. Here, we report that MOV10 suppresses influenza A virus infection through interacting with viral nucleoprotein (NP), sequestering viral RNP in the cytoplasm and causing the degradation of viral vRNA. The antiviral activity of MOV10 depends on the integrity of P-bodies. We also found that the antiviral activity of MOV10 is partially countered by viral NS1 protein that interferes with the interaction of MOV10 with viral NP and causes MOV10 degradation through the lysosomal pathway. Moreover, NS1-defective influenza A virus is more susceptible to MOV10 restriction. Our data not only expand the antiviral spectrum of MOV10 but also reveal the NS1 protein as the first viral antagonist of MOV10.


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