HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Maheshwari, R. K. Articles by Friedman, R. M. Search for Related Content PubMed PubMed Citation Articles by Maheshwari, R. K. Articles by Friedman, R. M. Agricola Articles by Maheshwari, R. K. Articles by Friedman, R. M.

Primary amines enhance the antiviral activity of interferon against a membrane virus: role of intracellular pH

Department of Pathology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814-4799, U.S.A.

Inhibition of vesicular stomatitis virus (VSV) replication in L_B cells by interferon (IFN) resembles the action of IFN on some retroviruses, in that the incorporation of glycoprotein into virions is defective. Primary amines added between 1 and 2 h post-infection significantly enhanced (five- to 1000-fold) the antiviral activity of IFN against VSV, but no enhancement of the antiviral activity of IFN against encephalomyocarditis virus, a virus with no membrane component, by primary amines was seen. SDS-PAGE and immunofluorescence analysis of viral proteins, and Nycodenz gradient fractionation, suggested that both IFN and primary amines inhibited the transport of VSV glycoprotein (G) to the plasma membrane; instead, G accumulated in the trans-Golgi network (TGN). Using sensitive intracellular pH (pHi) indicators, we found that IFN treatment significantly raised the pHi. A further increase in pHi was seen with a combination of IFN and primary amines; the increase in pHi correlated with an enhancement of the antiviral activity of IFN by primary amines. Amiloride inhibited the IFN-induced increase in pHi and a concomitant increase in the concentration of Na⁺ ions; this observation suggested that IFN induced cytoplasmic alkalinization by activating an Na⁺/H⁺ antiporter system. These results indicated that the IFN-induced increase in pHi may be responsible for the accumulation of G in the TGN, thereby producing G-deficient virus particles with reduced infectivity.

Received 7 January 1991; accepted 10 May 1991.

This article has been cited by other articles:

				D.F. FERREIRA, M.P. E. SANTO, M.A. REBELLO, and M.C. S. REBELLO Weak bases affect late stages of Mayaro virus replication cycle in vertebrate cells J. Med. Microbiol., April 1, 2000; 49(4): 313 - 318. [Abstract] [Full Text] [PDF]

				L. M. Maglova, W. E. Crowe, P. R. Smith, A. A. Altamirano, and J. M. Russell Na+-K+-Cl- cotransport in human fibroblasts is inhibited by cytomegalovirus infection Am J Physiol Cell Physiol, November 1, 1998; 275(5): C1330 - C1341. [Abstract] [Full Text] [PDF]