Effects of Adenosine Monophosphate on the Reactivation of Latent Herpes Simplex Virus Type 1 Infections of Mice

Blue, William T.; Winland, Roger D; Stobbs, Darlene G.; Kirksey, D.F.; Savage, Russell E.

doi:10.1128/aac.20.4.547

Cited by 10 publications

(4 citation statements)

References 8 publications

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“…The capacity of AMP to prevent both primary and recurrent herpes simplex virus type 1 (HSV- 1) infections resulting from inoculation of mouse ear pinnae has been previously reported (1). Here we report the results of therapeutic trials carried out in the same animal model system.…”

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confidence: 65%

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Activity of AMP against experimental herpes simplex virus type 1 infections in mice

Blue¹,

Macias²,

Sklar³

1983

Antimicrob Agents Chemother

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Administration of AMP soon after inoculation of mice with herpes simplex virus type 1 inhibited development of virus-induced lesions and appeared to prevent establishment of virus latency. These effects were dependent on both the AMP dose and the time of AMP administration. Regression of herpes simplex virus type 1-induced lesions was also accelerated significantly by AMP treatment in a timeand dose-dependent manner.The capacity of AMP to prevent both primary and recurrent herpes simplex virus type 1 (HSV-1) infections resulting from inoculation of mouse ear pinnae has been previously reported (1). Here we report the results of therapeutic trials carried out in the same animal model system. These investigations were prompted by several reports indicating possible antiviral activities inherent in adenosine or AMP (5, 10-12), as well as by a growing list of reported pharmacological and physiological effects of adenosine and AMP (2-4, 6, 9).The mouse ear pinnae model of Hill et al. (7,8) A multiple-dose treatment regimen (four doses over a 24-h period) was used to determine the minimum dose required to completely inhibit the formation of primary lesions. AMP (Sigma Chemical Co., St. Louis, Mo.) was dissolved in phosphate-buffered saline (pH 7.4) just before use and administered intraperitoneally. Nine groups of mice received AMP at 1, 6, 12, and 24 h after inoculation with HSV-1. The individual dose required to reduce the incidence of primary ear lesions by at least 50% was 2.0 mg/kg; the total dose was 8.0 mg/kg (Table 1). The minimum 100% inhibitory dose was 10 mg/kg, or a total of 40 mg/kg over 24 h.

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confidence: 65%

“…The mouse ear pinnae model of Hill et al (7,8) was utilized as described previously (1). For primary infection, the right ear pinnae of 4- A multiple-dose treatment regimen (four doses over a 24-h period) was used to determine the minimum dose required to completely inhibit the formation of primary lesions.…”

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confidence: 99%

Activity of AMP against experimental herpes simplex virus type 1 infections in mice

Blue¹,

Macias²,

Sklar³

1983

Antimicrob Agents Chemother

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“…Thus, we hypothesize that functional ADORA2A is required for the survival of SNU719 cells. A previous study reported that AMP could prevent the establishment of a latent infection and eradicate latent HSV-1 from the central nervous system [37]. This eradication of latent HSV-1 might be related to HSV-1 lytic reactivation.…”

Section: Discussionmentioning

confidence: 99%

Adenosine Induces EBV Lytic Reactivation through ADORA1 in EBV-Associated Gastric Carcinoma

Choi

Ryu

Lee

et al. 2019

IJMS

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Cordyceps species are known to contain numerous bioactive compounds, including cordycepin. Extracts of Cordyceps militaris (CME) are used in diverse medicinal purposes because of their bioactive components. Cordycepin, one of the active components of CME, exhibits anti-proliferative, pro-apoptotic, and anti-inflammatory effects. Cordycepin structurally differs from adenosine in that its ribose lacks an oxygen atom at the 3′ position. We previously reported that cordycepin suppresses Epstein–Barr virus (EBV) gene expression and lytic replication in EBV-associated gastric carcinoma (EBVaGC). However, other studies reported that cordycepin induces EBV gene expression and lytic reactivation. Thus, it was reasonable to clarify the bioactive effects of CME bioactive compounds on the EBV life cycle. We first confirmed that CME preferentially induces EBV gene expression and lytic reactivation; second, we determined that adenosine in CME induces EBV gene expression and lytic reactivation; third, we discovered that the adenosine A1 receptor (ADORA1) is required for adenosine to initiate signaling for upregulating BZLF1, which encodes for a key EBV regulator (Zta) of the EBV lytic cycle; finally, we showed that BZLF1 upregulation by adenosine leads to delayed tumor development in the EBVaGC xenograft mouse model. Taken together, these results suggest that adenosine is an EBV lytic cycle inducer that inhibits EBVaGC development.

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“…Other observations suggest that cyclic nucleotides might also be involved in cellular control of the latent infection. 163 The existence of control mechanisms of cyclic nucleotides for selection of gene expression leading to induction of viral replication in somatic cell hybrids carrying but not expressing EBV genomes has been described. 164 Conversion of productive measles virus infection in neural cells to low or nonproductive infections may be achieved by treatment with drugs capable of modifying cyclic nucleotide metabolism.…”

Section: Influences Of the Cns And Neural Cells On Virus Infectionsmentioning

confidence: 99%

Virus-Induced Changes in Neural Cells

Lycke¹

1985

Pathological Neurochemistry

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Effects of Adenosine Monophosphate on the Reactivation of Latent Herpes Simplex Virus Type 1 Infections of Mice

Abstract: Adenosine monophosphate pretreatment of mice with latent herpes simplex virus type 1 infections significantly reduced the rate of reactivation of latent virus. Adenosine monophosphate pretreatment did not, however, eradicate latent virus.Recently,

Cited by 10 publications

References 8 publications

Activity of AMP against experimental herpes simplex virus type 1 infections in mice

Activity of AMP against experimental herpes simplex virus type 1 infections in mice

Adenosine Induces EBV Lytic Reactivation through ADORA1 in EBV-Associated Gastric Carcinoma

Virus-Induced Changes in Neural Cells

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