Chromatin control of herpes simplex virus lytic and latent infection

Knipe, David M.; Cliffe, Anna R.

doi:10.1038/nrmicro1794

Cited by 382 publications

(411 citation statements)

References 126 publications

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“…Since PAA inhibits viral DNA polymerase activity, it is speculated that the CAF1 aggregation forms after the onset of viral DNA synthesis, which fits the function of CAF1 in transferring H3/H4 dimer onto newly synthesized DNA. Nevertheless, the model is likely specific to HCMV, as its close neighbors, the HSVs, replicate in the compartments that exclude histones, even though their genome associates with histones in infected cells [63].…”

Section: Discussionmentioning

confidence: 99%

Host-viral effects of chromatin assembly factor 1 interaction with HCMV IE2

Lee

et al. 2011

Cell Res

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Chromatin assembly factor 1 (CAF1) consisting of p150, p60 and p48 is known to assemble histones onto newly synthesized DNA and thus maintain the chromatin structure. Here, we show that CAF1 expression was induced in human cytomegalovirus (HCMV)-infected cells, concomitantly with global chromatin decondensation. This apparent conflict was thought to result, in part, from CAF1 mislocalization to compartments of HCMV DNA synthesis through binding of its largest subunit p150 to viral immediate-early protein 2 (IE2). p150 interaction with p60 and IE2 facilitated HCMV DNA synthesis. The IE2Q548R mutation, previously reported to result in impaired HCMV growth with unknown mechanism, disrupted IE2/p150 and IE2/histones association in our study. Moreover, IE2 interaction with histones partly depends on p150, and the HCMV-induced chromatin decondensation was reduced in cells ectopically expressing the p150 mutant defective in IE2 binding. These results not only indicate that CAF1 was hijacked by IE2 to facilitate the replication of the HCMV genome, suggesting chromatin assembly plays an important role in herpesviral DNA synthesis, but also provide a model of the virus-induced chromatin instability through CAF1.

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Section: Discussionmentioning

confidence: 99%

Host-viral effects of chromatin assembly factor 1 interaction with HCMV IE2

Lee

et al. 2011

Cell Res

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“…In order to establish and maintain latency, a number of complex processes must be balanced. These include silencing of viral lytic-phase genes, abrogation of host cellular defense mechanisms (e.g., apoptosis), and evasion of host immunity, including both innate and acquired immune responses (e.g., suppression of major histocompatibility complex expression) [35,36]. HSV-specific CD8+ T cells take up residence in the trigeminal ganglia and contribute to maintaining the virus in the latent state [37].…”

Section: Introductionmentioning

confidence: 99%

Herpes Simplex Virus-1 Encephalitis in Adults: Pathophysiology, Diagnosis, and Management

2016

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Herpetic infections have plagued humanity for thousands of years, but only recently have advances in antiviral medications and supportive treatments equipped physicians to combat the most severe manifestations of disease. Prompt recognition and treatment can be lifesaving in the care of patients with herpes simplex-1 virus encephalitis, the most commonly identified cause of sporadic encephalitis worldwide. Clinicians should be able to recognize the clinical signs and symptoms of the infection and familiarize themselves with a rational diagnostic approach and therapeutic modalities, as early recognition and treatment are key to improving outcomes. Clinicians should also be vigilant for the development of acute complications, including cerebral edema and status epilepticus, as well as chronic complications, including the development of autoimmune encephalitis associated with antibodies to the N-methyl-D-aspartate receptor and other neuronal cell surface and synaptic epitopes. Herein, we review the pathophysiology, differential diagnosis, and clinical and radiological features of herpes simplex virus-1 encephalitis in adults, including a discussion of the most common complications and their treatment. While great progress has been made in the treatment of this life-threatening infection, a majority of patients will not return to their previous neurologic baseline, indicating the need for further research efforts aimed at improving the long-term sequelae.

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“…This new work provides physical evidence that herpes-like particles are produced in coral tissues (Figure 4a). Given their cosmopolitan presence in healthy individuals of every coral genus tested (for example, Porites, Acropora, Montastraea and Diploria), we hypothesize that herpes-like viruses establish Viruses associated with diseased corals N Soffer et al long-term non-fatal infections in corals, in a manner similar to their infections of vertebrate hosts (Knipe and Cliffe, 2008). …”

Section: Herpesviruses Dominate Healthy Tissuesmentioning

confidence: 99%

Potential role of viruses in white plague coral disease

Soffer

Brandt

Correa³

et al. 2013

The ISME Journal

107

121

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White plague (WP)-like diseases of tropical corals are implicated in reef decline worldwide, although their etiological cause is generally unknown. Studies thus far have focused on bacterial or eukaryotic pathogens as the source of these diseases; no studies have examined the role of viruses. Using a combination of transmission electron microscopy (TEM) and 454 pyrosequencing, we compared 24 viral metagenomes generated from Montastraea annularis corals showing signs of WP-like disease and/or bleaching, control conspecific corals, and adjacent seawater. TEM was used for visual inspection of diseased coral tissue. No bacteria were visually identified within diseased coral tissues, but viral particles and sequence similarities to eukaryotic circular Rep-encoding single-stranded DNA viruses and their associated satellites (SCSDVs) were abundant in WP diseased tissues. In contrast, sequence similarities to SCSDVs were not found in any healthy coral tissues, suggesting SCSDVs might have a role in WP disease. Furthermore, Herpesviridae gene signatures dominated healthy tissues, corroborating reports that herpes-like viruses infect all corals. Nucleocytoplasmic large DNA virus (NCLDV) sequences, similar to those recently identified in cultures of Symbiodinium (the algal symbionts of corals), were most common in bleached corals. This finding further implicates that these NCLDV viruses may have a role in bleaching, as suggested in previous studies. This study determined that a specific group of viruses is associated with diseased Caribbean corals and highlights the potential for viral disease in regional coral reef decline.

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Chromatin control of herpes simplex virus lytic and latent infection

Cited by 382 publications

References 126 publications

Host-viral effects of chromatin assembly factor 1 interaction with HCMV IE2

Host-viral effects of chromatin assembly factor 1 interaction with HCMV IE2

Herpes Simplex Virus-1 Encephalitis in Adults: Pathophysiology, Diagnosis, and Management

Potential role of viruses in white plague coral disease

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