Human cytomegalovirus persists in cells treated with interferon

Rodríguez, José; Loepfe, T. R.; Stinski, Mark F.

doi:10.1007/bf01309276

Cited by 7 publications

(10 citation statements)

References 7 publications

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“…Addition of interferon to infected cultures has been shown to be effective in maintaining a persistent infection (2,14). However, no interferon-like activity could be detected in our persistently infected PA~ cultures.…”

Section: T H E M a J O R I T Y Of S U C H Cells W E R E P O S I T I Vcontrasting

confidence: 64%

Latent infection of human ovarian teratocarcinoma cells with human cytomegalovirus

Kamiya

Tanaka

Ogura

et al. 1986

Archives of Virology

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Persistent infection with human cytomegalovirus (HCMV) can be established in cultures of human ovarian teratocarcinoma (PA1) cells, and maintained for more than 200 days. Infected cultures maintained at 34 degrees C (PA1CMV34) and 37 degrees C (PA1CMV37) entered crisis and subsequently displayed massive cytopathic effects (CPE), whereas infected cultures maintained at 32 degrees C (PA1CMV32) and 39 degrees C (PA1CMV39) continued to release small amounts of infectious virus until 240 or 151 days post-infection (p.i.) respectively. PA1CMV32 cultures shifted to 37 degrees C at 258 days p.i. resumed synthesis of infectious virus which resulted in cell destruction, indicating that latent infection with HCMV was maintained in PA1 cells at 32 degrees C. In contrast, PA1CMV39 cells did not produce infectious virus even when cultured at 37 degrees C for more than 100 days after the temperature shift.

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Section: T H E M a J O R I T Y Of S U C H Cells W E R E P O S I T I Vcontrasting

confidence: 64%

Latent infection of human ovarian teratocarcinoma cells with human cytomegalovirus

Kamiya

Tanaka

Ogura

et al. 1986

Archives of Virology

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“…It has previously been reported that inhibition of HCMV replication in human fibroblast cultures derived from foreskin biopsies by IFNα was reversible [4], similar to observations made upon infection of several murine cell types with MCMV, including fibroblastic murine cells [24–26]. Reversible inhibition of HCMV replication would not be advantageous to many therapeutic strategies.…”

Section: Resultsmentioning

confidence: 87%

“…More recent studies have strongly indicated that the type I interferon response is inhibitory to HCMV replication. This data includes a report where HCMV secretion was inhibited upon administration of IFNα to patients [7], several reports indicating that pre-treatment of cells before infection in vitro with type I interferon proteins restricted HCMV replication [4, 8–11], and the observation that inhibition of type I interferon signalling allows greater replication of HCMV in vitro [12]. Additionally, numerous reports of HCMV-encoded mechanisms to antagonize interferon production, antagonize interferon signalling or antagonize the function of anti-viral proteins expressed in response to interferon emphasize that the type I interferon response is a barrier to HCMV replication [13–15].…”

Section: Introductionmentioning

confidence: 99%

“…This includes exploring the use of different interferon proteins to inhibit HCMV replication, as there may be multiple interferon proteins capable of inhibiting HCMV replication. Plus, there are aspects of interferon action on HCMV replication which have not been recently revisited, such as the possible reversible inhibition of HCMV replication in the presence and absence of interferon [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

“…Additionally, there may be long-standing observations about the interaction of HCMV and interferons that may need to be revisited to understand how those proteins can be used in a therapeutic setting. A previous study examining treatment of HCMV-infected human fibroblast cell cultures from foreskin biopsies with type I interferon indicated that inhibition of HCMV replication was reversible [ 4 ]. Similar observations have been made upon infection of murine cells, including fibroblastic murine cells, with a betaherpesvirus related to HCMV; murine cytomegalovirus (MCMV) [ 24–26 ].…”

Section: Introductionmentioning

confidence: 99%

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Inhibition of human cytomegalovirus replication by interferon alpha can involve multiple anti-viral factors

Chowdhury,

Latham,

Tran

et al. 2023

Journal of General Virology

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The shortcomings of current direct-acting anti-viral therapy against human cytomegalovirus (HCMV) has led to interest in host-directed therapy. Here we re-examine the use of interferon proteins to inhibit HCMV replication utilizing both high and low passage strains of HCMV. Pre-treatment of cells with interferon alpha (IFNα) was required for robust and prolonged inhibition of both low and high passage HCMV strains, with no obvious toxicity, and was associated with an increased anti-viral state in HCMV-infected cells. Pre-treatment of cells with IFNα led to poor expression of HCMV immediate-early proteins from both high and low passage strains, which was associated with the presence of the anti-viral factor SUMO-PML. Inhibition of HCMV replication in the presence of IFNα involving ZAP proteins was HCMV strain-dependent, wherein a high passage HCMV strain was obviously restricted by ZAP and a low passage strain was not. This suggested that strain-specific combinations of anti-viral factors were involved in inhibition of HCMV replication in the presence of IFNα. Overall, this work further supports the development of strategies involving IFNα that may be useful to inhibit HCMV replication and highlights the complexity of the anti-viral response to HCMV in the presence of IFNα.

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Beta interferon production in primed and unprimed cells infected with human cytomegalovirus

Rodríguez

Loepfe

Swack

1987

Archives of Virology

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Human cytomegalovirus induced beta interferon in cultures of human foreskin cells. The inhibitor was first released between 8 and 16 hours after infection, about 48 hours before progeny virus. In cultures infected with low concentrations of virus, interferon was produced as the infection spread, and then in amounts larger than expected. After infection with cytomegalovirus, cells which had been primed for 48 hours with purified beta interferon produced significantly more interferon than unprimed cells, and the interferon was produced earlier, between 2 and 8 hours after infection. CMV-induced interferon also was able to prime cells. The data suggest that the relatively large quantities of interferon detected in cultures infected with low concentrations of cytomegalovirus result from endogenous priming: those cells infected early first produce interferon which primes uninfected cells, then virus which induces the primed cells to produce interferon in relatively high concentrations.

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Human cytomegalovirus persists in cells treated with interferon

Abstract: Human cytomegalovirus disappeared from cultures continuously exposed to interferon. When interferon was removed, high titers of virus reappeared. Cytomegalovirus was thus able to persist in potentially infectious form in cells protected by interferon.

Cited by 7 publications

References 7 publications

Latent infection of human ovarian teratocarcinoma cells with human cytomegalovirus

Latent infection of human ovarian teratocarcinoma cells with human cytomegalovirus

Inhibition of human cytomegalovirus replication by interferon alpha can involve multiple anti-viral factors

Beta interferon production in primed and unprimed cells infected with human cytomegalovirus

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