Effects of tumor necrosis factor-α treatment on mortality in murine cytomegalovirus-infected mice

Anderson, Kevin; Lie, Yolanda; Low, Mari-Anne L.; Fennie, Elizabeth H.

doi:10.1016/0166-3542(93)90012-8

Cited by 14 publications

(9 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Importantly, our findings may help resolve a discrepancy in the literature regarding the importance of TNF-␣ in controlling MCMV infection. Consistent with findings by Anderson et (1), our data provide a mechanistic basis for the absence of a therapeutic benefit when giving TNF-␣ postinfection and may explain why the protective effects of TNF-␣ are observed only under specific experimental conditions (1,38,43). It is interesting that MCMV inhibits both IFN-␥ and TNF-␣ signaling.…”

Section: T-3ј) and Traf1_r (5ј-gagtcgcagactgtgctc-3ј)supporting

confidence: 77%

“…One study has shown that TNF-␣ pretreatment is protective in vivo, in synergy with IFN-␥ (18). Treatment after MCMV infection resulted in increased mortality, illustrating that TNF-␣ is a two-edged sword (1). Interestingly, studies with HCMV have also revealed conflicting roles for cytokines such as TNF-␣ and IFN-␥ in controlling viral infection in some situations (10,11,26) but not others (41).…”

mentioning

confidence: 99%

“…Generally, these cytokines are thought to be protective through direct antiviral action and/or indirectly by orchestrating the immune response. Several studies illustrate the protective effects of TNF-␣ pretreatment in vitro (1,18,43), but the effects of TNF-␣ in vivo are less clear. Several laboratories have used antibodies or soluble TNF receptors to deplete TNF-␣ in vivo, resulting in enhanced MCMV disease (12,15,28,30).…”

mentioning

confidence: 99%

See 2 more Smart Citations

Murine Cytomegalovirus Infection Inhibits Tumor Necrosis Factor Alpha Responses in Primary Macrophages

Popkin

Virgin

2003

J Virol

View full text Add to dashboard Cite

Despite robust host immune responses the betaherpesvirus murine cytomegalovirus (MCMV) is able to establish lifelong infection. This capacity is due at least in part to the virus utilizing multiple immune evasion mechanisms to blunt host responses. Macrophages are an important cell for MCMV infection, dissemination, and latency despite expression in the host of multiple cytokines, including tumor necrosis factor alpha (TNF-␣), that can induce an antiviral state in macrophages or other cells. In this study, we found that MCMV infection of bone marrow-derived macrophages inhibited TNF-␣-induced ICAM-1 surface expression and mRNA expression in infected cells via expression of immediate early and/or early viral genes. MCMV infection blocked TNF-␣-induced nuclear translocation of NF-B. This inhibition of TNF-␣ signaling was explained by a decrease in TNF receptor 1 (TNFR1) and TNFR2 that was due to decreased mRNA for the latter. These findings provide a mechanism by which MCMV can evade the effects of an important host cytokine in macrophages.

show abstract

Section: T-3ј) and Traf1_r (5ј-gagtcgcagactgtgctc-3ј)supporting

confidence: 77%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Murine Cytomegalovirus Infection Inhibits Tumor Necrosis Factor Alpha Responses in Primary Macrophages

Popkin

Virgin

2003

J Virol

View full text Add to dashboard Cite

show abstract

“…TNF-␣ can directly, or synergistically with IFN-␥, inhibit MCMV replication in vitro (29, 55). TNF-␣ has also been reported to limit MCMV replication and pathology (24, 33) and enhance the protective effects of IFN-␥ against lethal infection (1). However, other studies have found no effect of TNF-␣ on the acute phase of MCMV infection in vivo (49,55) and NK cells are not required for production of TNF-␣ during MCMV infection (33, 35).…”

Section: Fig 3 Pfp and Ifn-␥ Are Important For Protection Against Lmentioning

confidence: 86%

Natural Killer Cells Utilize both Perforin and Gamma Interferon To Regulate Murine Cytomegalovirus Infection in the Spleen and Liver

Loh¹,

Chu

O’Guin³

et al. 2005

J Virol

151

139

View full text Add to dashboard Cite

“…[8][9][10][11][12] FHF is associated with high serum levels of TNF-␣, so enhanced viral replication in patients with FHF may be mediated by TNF-␣. Sheron et al 13 observed very high levels of TNF-␣ in the serum of patients with FHF.…”

Section: Discussionmentioning

confidence: 99%

Enhanced (cytomegalovirus) viral replication after transplantation for fulminant hepatic failure

et al. 1997

View full text Add to dashboard Cite

Fulminant hepatic failure (FHF) is an established indication for liver transplantation. A pretransplant diagnosis of FHF may be a risk factor for subsequent development of cytomegalovirus (CMV) infection, although the mechanism of this association is not understood. FHF is associated with very high levels of tumor necrosis factor ␣ (TNF-␣), and TNF-␣ may directly promote viral replication. We have used the polymerase chain reaction (PCR) to examine sequentially collected buffy coats from 106 consecutive adult liver transplant recipients. PCR evidence of CMV replication was found for 13 of 18 patients who underwent transplantation for FHF (c.f. 23/88 non-FHF patients; P Ͻ .01). Ten of 12 patients who received transplants transplanted for fulminant seronegative hepatitis were buffy-coat PCR-positive, sometimes during the first posttransplant week. TNF-␣ was measured by enzyme-linked immunosorbent assay in selected sera, and results were examined in the context of a quantitative PCR assay. Serum TNF-␣ levels increased and decreased in concert with viral titers. High levels of TNF-␣ were not found in the early posttransplant period. We conclude that FHF (in particular, seronegative hepatitis) is associated with enhanced CMV replication in the posttransplant period. Results also suggest that viral replication may be enhanced before transplantation. These patients may be at special risk for development of symptomatic CMV infection.

show abstract

Effects of tumor necrosis factor-α treatment on mortality in murine cytomegalovirus-infected mice

Cited by 14 publications

References 24 publications

Murine Cytomegalovirus Infection Inhibits Tumor Necrosis Factor Alpha Responses in Primary Macrophages

Murine Cytomegalovirus Infection Inhibits Tumor Necrosis Factor Alpha Responses in Primary Macrophages

Natural Killer Cells Utilize both Perforin and Gamma Interferon To Regulate Murine Cytomegalovirus Infection in the Spleen and Liver

Enhanced (cytomegalovirus) viral replication after transplantation for fulminant hepatic failure

Contact Info

Product

Resources

About