Phospholipids in newcastle disease virus infected cells

Israël, Alain; Audubert, François; Semmel, Marianne

doi:10.1016/0005-2736(75)90191-1

Cited by 5 publications

(5 citation statements)

References 18 publications

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“…Non-cell-associated viruses have also been reported to alter cellular lipid components: glycolipid, phospholipid, and sphingolipid with herpes simplex virus infection (12,25,27,28); phospholipid and phospholipid precursors with infections of Newcastle disease virus, fowl plaque virus, and Semliki Forest virus (8,17); glycolipids with poxvirus infection (3); phospholipids with Sendai virus infection (5); phospholipid fatty acid composition with cells persistently infected with measles virus (4); and neutral lipid and lipidbound sialic acid in monolayers infected with rabies virus (22). This is not the first report of variation in VZV strains.…”

Section: Resultsmentioning

confidence: 99%

Differentiation of strains of varicella-zoster virus by changes in neutral lipid metabolism in infected cells

Jerkofsky¹,

Siervo²

1986

J Virol

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Eleven isolates of varicella-zoster virus were tested for their effects on the incorporation of [14C]acetate into lipids in infected human embryonic lung cells. By relative percent, all virus isolates demonstrated a shift from polar lipid synthesis to neutral lipid, especially triglyceride, synthesis. By data expressed as counts per minute per microgram of protein, the VZV strains could be separated into two groups: those strains which depressed lipid synthesis and those strains which did not depress, and may even have stimulated, lipid, especially triglyceride, synthesis. These results may be useful in understanding the development of lipid changes seen in children affected with Reye's syndrome following chickenpox. The human herpesvirus varicella-zoster virus (VZV) is the etiologic agent for the childhood disease of chickenpox (varicella) and the recurrent disease shingles (zoster) (30). Although the disease is rarely life threatening in normal children, problems occur in children whose immune systems are compromised. Clinical trials of an attenuated virus vaccine in susceptible children with leukemia are in progress (15). A serious sequel of chickenpox in normal children is Reye's syndrome (23). Following apparent recovery from an initial viral illness (influenza B in epidemic cases, chickenpox in endemic cases [9]), the child develops the symptoms of Reye's syndrome: projectile vomiting, cerebral edema, and fatty infiltration of the viscera. At the present time, there is no accepted mechanism to explain this syndrome, although several hypotheses have been proposed. Since Reye's syndrome can follow chickenpox and involves changes in lipid metabolism in the affected child, we examined the effects of various isolates of VZV on the lipid metabolism of infected human cells. MATERIALS AND METHODS Cell cultures. The MRC-5 line of human embryonic lung cells, obtained from Whittaker M. A. Bioproducts, Walkersville, Md., was grown and maintained in Eagle minimal essential medium supplemented with 5% fetal bovine serum, 5% newborn calf serum, 0.2% NaHCO3, 100 U of penicillin per ml, and 100 jig of streptomycin per ml (GIBCO Laboratories, Grand Island, N.Y.). Viruses. Eleven strains of VZV were used in these studies. Four strains were obtained from P. Brunell, University of Texas Health Science Center at San Antonio: Ellen (EL), Lozano 26 (L26), Lozano 28 (L28), and Gretchen (GR). Two strains were obtained from S. Strauss and J. Ostrove at the National Institutes of Health: D. Luzak (DL) and Oka (OB). Five strains were isolated from clinical specimens in our laboratory: PVWT (PV), HSWT (HS), LCWT (LC), WT1 (WT), and JBWT (JB). Viruses were tested between passages 3 and 14. All virus strains were maintained as cellassociated virus in MRC-5 cells. Virus stocks were stored at-85°C. Initial studies determined that there was no signifi-* Corresponding author.

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Section: Resultsmentioning

confidence: 99%

Differentiation of strains of varicella-zoster virus by changes in neutral lipid metabolism in infected cells

Jerkofsky¹,

Siervo²

1986

J Virol

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“…These differences were observed at times when the relative proportions of newly labeled phospholipids were not yet stabilized. As has been described elsewhere [13], each phospholipid has a different turnover and the relative proportions of labeled phospholipids become stable only after 48 h.…”

Section: Resultsmentioning

confidence: 99%

“…In cells infected with lipovirus PM2, phosphatidylethanolamine synthesis in creases and phosphatidylglycerol synthesis decreases 1 h after infection [11], On infecting BHK cells with Semliki Forest virus, phosphatidylcholine syn thesis is inhibited, due to the inhibition of 1,2-diglyceride choline-phospho transferase [12]. In chorioallantoic membrane cells (CAM) and chick embryo cells (CEC) infected with NDV, phosphatidylserine synthesis increases and phosphatidylcholine synthesis decreases 4 h after infection [13].…”

mentioning

confidence: 99%

Effect of Virus Infection and Cycloheximide Treatment on the Labeling of Cellular Phospholipids with <sup>32</sup>P

Audubert¹,

Semmel²

1977

Intervirology

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The total amount and the relative proportions of labeled phospholipids were studied in chorioallantoic membrane cells (CAM), chick embryo cells (CEC) and L cells which were either infected with Newcastle disease virus (NDV), fowl plague virus (FPV) and mouse encephalomyocarditis (EMC) virus or treated with cycloheximide. In productively infected or nonproductively infected cells, the total amount of labeled phospholipids was not altered, but the relative proportions of individual phospholipids were modified. These modifications were related to the presence of viral proteins. Blocking of protein synthesis for 6 h with 7 µg cycloheximide/ml did not modify the total amount of labeled phospholipids in CAM and CEC. Less label was incorporated into cycloheximide-treated L cells than in controls. The relative proportions of the labeled individual phospholipids were modified in all three cell types and these modifications were different from those in virus-infected cells.

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“…Data presented in Table 6 show few statistical differences between the amounts of fatty acids found at 3k C as compared to those at 39 C. Variation between infected and non-infected cultures were independent of temperature. This is under standable because enveloped animal viruses have been shown to modify host cell lipid synthesis (Blair and Brennan, 1972;Shibuta and Matumoto, 1972;Israel et al, 1975)'…”

Section: Discussionmentioning

confidence: 99%

Studies on the factors involved during the maturation of Newcastle disease virus

Burdick

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Phospholipids in newcastle disease virus infected cells

Cited by 5 publications

References 18 publications

Differentiation of strains of varicella-zoster virus by changes in neutral lipid metabolism in infected cells

Differentiation of strains of varicella-zoster virus by changes in neutral lipid metabolism in infected cells

Effect of Virus Infection and Cycloheximide Treatment on the Labeling of Cellular Phospholipids with <sup>32</sup>P

Studies on the factors involved during the maturation of Newcastle disease virus

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