Herpesvirus latency confers symbiotic protection from bacterial infection

  title={Herpesvirus latency confers symbiotic protection from bacterial infection},
  author={Erik S. Barton and Douglas W White and Jason S. Cathelyn and Kelly A. Brett-McClellan and Michael Engle and Michael Steven Diamond and Virginia L. Miller and Herbert W. Virgin},
All humans become infected with multiple herpesviruses during childhood. After clearance of acute infection, herpesviruses enter a dormant state known as latency. Latency persists for the life of the host and is presumed to be parasitic, as it leaves the individual at risk for subsequent viral reactivation and disease. Here we show that herpesvirus latency also confers a surprising benefit to the host. Mice latently infected with either murine gammaherpesvirus 68 or murine cytomegalovirus… 
Immune modulation during latent herpesvirus infection
This review explores data in human and animal systems that reveal the ability of latent herpesviruses to modulate the immune response to self and environmental antigens and forces us to reconsider what constitutes a ‘normal’ immune system in a healthy individual.
Herpesviruses: latency and reactivation – viral strategies and host response
  • B. Grinde
  • Medicine, Biology
    Journal of oral microbiology
  • 2013
The review starts by introducing possible viral strategies in general and the particular biology and host relationship of the various human herpesviruses, including their pathology, are examined subsequently.
gamma-Herpesvirus-induced protection against bacterial infection is transient.
It is confirmed that latent gammaHV68 infection confers protection against subsequent infection with Listeria monocytogenes, however, the effect is transient, lasting only a few months.
Importance of Antibody in Virus Infection and Vaccine-Mediated Protection by a Latency-Deficient Recombinant Murine γ-Herpesvirus-68
The immune correlates of AC-RTA–mediated protection are examined and it is shown that sterilizing immunity requires both T cells and Ab, and important considerations in the development of vaccination strategies based on live-attenuated viruses are highlighted.
MHV68 Latency Modulates the Host Immune Response to Influenza A Virus
Mice latently infected with MHV68 showed significantly higher survival to influenza A virus infection than did PBS mock-infected mice, and activated alveolar macrophages are a key mechanistic component in protection from secondary infections.
Gammaherpesvirus Latency Differentially Impacts the Generation of Primary versus Secondary Memory CD8+ T Cells during Subsequent Infection
The results suggest that unlike pathogen-free laboratory mice, infection or immunization of latently infected humans may result in the generation of T cells with limited potential for long-term protection.
Simultaneous infection with gammaherpes and influenza viruses enhances the host immune defense.
It is unambiguous that lower MHV-68 expression was detected in lungs and peritoneal exudate cells from 3rd to 10th day after co-infection with IAV, and co- Infection with herpes and influenza viruses could be mutually beneficial for the host by promoting its defense against both viruses.
Helminth infection reactivates latent γ-herpesvirus via cytokine competition at a viral promoter
Chronic herpesvirus infection, a component of the mammalian virome, is regulated by the counterpoised actions of multiple cytokines on viral promoters that have evolved to sense host immune status.
Virus reactivation: a panoramic view in human infections.
This article examines the published literature and current knowledge regarding the viral and cellular proteins that may play a role in viral reactivation and those viruses known to cause latent infections, which include herpes simplex virus, varicella zoster virus, Epstein-Barr virus, human cytomegalovirus, human herpesvirus 7, Kaposi's sarcoma-associated herpesv virus, JC virus, BK virus, parvovirus and adenovirus.


Establishment and Maintenance of Gammaherpesvirus Latency Are Independent of Infective Dose and Route of Infection
It is indicated that any initiation of infection leads to substantial acute-phase replication and subsequent establishment of a maximal level of latency, and infections with doses as small as 0.1 PFU of γHV68 result in stable levels of acute- phase replication and latent infection.
Immune Control of the Number and Reactivation Phenotype of Cells Latently Infected with a Gammaherpesvirus
It is demonstrated for the first time that CD8+ T cells regulate both latency and persistent replication and it is shown that gamma interferon and perforin are essential for immune control of latency and persistence.
The Gammaherpesvirus 68 Latency-Associated Nuclear Antigen Homolog Is Critical for the Establishment of Splenic Latency
Significant differences in the kinetics of induction of lethality in mice lacking B and T cells and the construction of a γHV68 mutant containing a translation termination codon in the LANA ORF suggest LANA appears to be a critical determinant in the establishment of γ HV68 latency in the spleen post-intranasal infection.
Preemptive CD8 T-Cell Immunotherapy of Acute Cytomegalovirus Infection Prevents Lethal Disease, Limits the Burden of Latent Viral Genomes, and Reduces the Risk of Virus Recurrence
The benefits and the limits of a preemptive CD8 T-cell immunotherapy ofCMV infection in the immunocompromised bone marrow transplantation recipient are demonstrated and the existence of an invariant, therapy-resistant load suggests a role for immune system evasion mechanisms in the establishment of CMV latency.
The conditions of primary infection define the load of latent viral genome in organs and the risk of recurrent cytomegalovirus disease
The presence of latent CMV in multiple organs provides the molecular basis for stochastic events of recurrence in single organs or in any combination thereof and provides a rationale for the diversity in the clinical outcome of CMV disease.
Tonsillar homing of Epstein-Barr virus-specific CD8+ T cells and the virus-host balance.
It is suggested that efficient control of EBV infection requires appropriate CD8+ T cell homing to oropharyngeal sites, and latent epitope reactivities were quicker than lytic reactivities both to acquire CCR7 and to accumulate in the tonsil.
Long-Term Latent Murine Gammaherpesvirus 68 Infection Is Preferentially Found within the Surface Immunoglobulin D-Negative Subset of Splenic B Cells In Vivo
It is demonstrated that latency is established in a variety of cell populations but that long-term latency in the spleen after intranasal inoculation predominantly occurs in B cells, and at late times postinfection latent γHV68 is largely confined to the surface immunoglobulin D-negative subset of B cells.
Critical Role of CD4 T Cells in an Antibody-Independent Mechanism of Vaccination against Gammaherpesvirus Latency
It is demonstrated here that antibody and B cells are not required for vaccination against latency, and that surveillance of latent infection in normal animals depends on CD4 and CD8 T cells, suggesting that T cells might be capable of preventing the establishment of latency.