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(Muhv 4) Strains: a Role for Immunomodulatory Proteins Encoded by the Left (5’-)End of the Genome

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(Muhv 4) Strains: a Role for Immunomodulatory Proteins Encoded by the Left (5’-)End of the Genome Cent. Eur. J. Biol. • 3(1) • 2008 • 19-30 DOI: 10.2478/s11535-008-0002-0 Central European Journal of Biology Comparison of pathogenic properties of the murid gammaherpesvirus (MuHV 4) strains: a role for immunomodulatory proteins encoded by the left (5’-)end of the genome Review Article Jela Mistríková1,2, Július Rajčáni2* 1 Department of Microbiology and Virology, Faculty of Microbiology and Natural Sciences, Comenius University, 84215 Bratislava, Slovakia 2 Institute of Virology, Slovak Academy of Sciences, 84505 Bratislava, Slovakia Received 13 September 2007; Accepted 4 January 2008 Abstract: The murid herpesvirus 4 (MuHV 4) species encompasses 7 isolates, out of which at least two (MHV-68, MHV-72) became in vitro propagated laboratory strains. Following intranasal inoculation, MuHV 4 induces an acute infectious mononucleosis-like syndrome with elevated levels of peripheral blood leukocytes, shifts in the relative proportion of lymphocytes along with the appearance of atypi- cal mononuclear cells. At least two isolates exhibited spontaneous deletions at the left hand (5´-end) of their genome, resulting in the absence of M1, M2, M3 genes (strain MHV-72) and also of the M4 gene (strain MHV-76). Based on DNA sequence amplifications only, another two isolates (MHV-Šum and MHV-60) were shown to possess similar deletions of varying length. During latency (until 24 months post-infection), the mice infected with any MuHV 4 isolate (except MHV-76) developed lymphoproliferative disorders. The lack of tumor formation in MHV-76 infected mice was associated with persistent virus production at late post-infection intervals. In addition to careful analysis of spontaneously occurring 5´-end genome defects, our knowledge of the function of 5´-end genes relies on the behaviour of mutants with corresponding deletions and/or insertions. While M2 and M3 genes encode immune evasion proteins, M4 codes for a soluble glycopeptide acting as immunomodulator and/or immunostimulator. Keywords: Murid gammaherpesvirus 4 • Genome deletions • Immune evasion genes • Pathogenesis • Tumor formation © Versita Warsaw and Springer-Verlag Berlin Heidelberg. Abbreviations 1. Introduction HSV - herpes simplex virus The history of murine herpesvirus goes back to 1980, i.n. - intranasal when several herpesvirus isolates (designated MHV-60; i.p. - intraperitoneal MHV-68; MHV-72; MHV-76; MHV-78, MHV-ŠUM) were p.i. - post-infection obtained from free-living Clethrionomys and Apodemus MHV - mouse herpesvirus (murine gammaherpesvirus) rodents captured in different regions of the former MuHV - murid herpesvirus (official nomenclature) Czechoslovakia [1,2]. All the MHV isolates grew well PCR - polymerase chain reaction in cell cultures of mouse, chick, rabbit, hamster, mink, bp - base pair swine, monkey or human origin (especially primary or kb - kilobase pair diploid embryonic cells), indicating that the new herpes nt(s) - nucleotide(s) virus was not a cytomegalovirus [3]. Later on Efstathiou w.t. - wild-type et al. [4] showed that the genome of MHV-68 had at least * E-mail: [email protected] 19 Comparison of pathogenic properties of the murid gammaherpesvirus (MuHV 4) strains: a role for immunomodulatory proteins encoded by the left (5’-)end of the genome 16 ORFs, which are homologous to Epstein Barr virus epithelial cells [13]. Using the latter model, the IgM (EBV) and to Herpesvirus saimiri sequences. Based deficient CD21-positive lymphocytes became latent on these data, the murine herpesvirus strain 68 (MHV- virus carriers at a lower frequency, since macrophages 68) was classified into genus Rhadinovirus, subfamily and NK cells formed the main cell population, in which Gammaherpesvirinae. All the above-mentioned isolates, the viral DNA survived. Obviously, in B cell-deficient which are serologically highly related [5], were classified mice, the B lymphocytes cannot account for latency [16]. as a single species of Murid herpesvirus 4 (MuHV 4) [6]. When adherent mononuclear cells (AMC) from infected Balb/c mice were T-cell depleted and enriched by means of the anti-macrophage F4/80 monoclonal antibody, this 2. Pathogenesis of the prototype strain AMC population was shown to contain MHV-68 DNA at MHV-68 in laboratory mice late p.i. intervals [17]. Thus, both lymphocytes as well as macrophages may represent the reservoir of latent Pilot studies with the MHV-68 strain showed that, in virus especially in adult animals, which did not undergo response to intranasal (i.n.) inoculation into outbred acute disease. mice, this virus spreads to the lungs and then via the The B lymphocytes producing MHV-68 or expressing bloodstream it reaches several internal organs such as MHV-68 antigen(s), may be cleared from blood, lymph the spleen, liver, and kidneys [7]. The survivors of acute nodes, spleen and lung alveoli by cytotoxic T/CD8 infection, especially adult and juvenile mice, developed cells. As a result of virus replication in the lungs, the T/ latent (and/or persistent) infection in the same organs. CD8 cells accumulate in the mediastinal lymph nodes In contrast to herpes simplex viruses (HSV 1 and 2), [18,19]. Mice depleted of T/CD8 cells failed to resolve the absence of neural spread was a striking feature [8]. the pulmonary disease, developed a long lasting viremia Though the MuHV 4 isolates are not strictly lymphotropic, and died; this confirms that T/CD8 lymphocytes are based on their genomic structure, the new isolates were essential for virus clearance. However, the cooperation classified as members of the Gammaherpesvirinae of CD8 lymphocytes with CD4 T cells is still required subfamily [4]. Using a combination of serology and for long-term protection [20,21]. MHV-68 infection may PCR analysis, Blasdell et al. [9] found that MuHV 4 also be associated with massive proliferation of those was endemic in wood mice (Apodemus sylvaticus) but lymphocytes that are not specific for this virus. The not in two species of voles (Clethrionomys glareolus, level of “bystander-induced” cycling in a population of Microtus agrestis). More recently, a longitudinal study of influenza virus-specific T/CD8+ cells was fourfold lower MuHV 4 antibody in a mixed ensemble of bank voles (C. than was the extent of cell division driven by the specific glareolus) and wood mice (A. sylvaticus) showed that the MHV-68 antigen [22]. latter represent the more frequent reservoir, even when Following i.n. MHV-68 inoculation, viremia occurs the virus was originally isolated from the former [10]. due to virus replication in the alveolar epithelium and Studies in Balb/c mice using MHV-68 demonstrated endothelial cells of alveolar septa at acute p.i. intervals. that the lung tissue becomes primarily involved following The productive virus growth within lung epithelium is i.n. inoculation [11]. Splenomegaly occurred in the resolved at 7 to 10 days p.i. During the viremic phase, course of acute infection as well as at late post-infection the mature B cells as well as macrophages become (p.i.) intervals among healthy survivors, in which B cells infected. In the course of primary infection, the T/CD8 were predominant virus carriers [12]. Depletion of T/CD4 cells (in cooperation with T/CD4 cells) proliferate to lymphocytes prevented splenomegaly, but had no effect participate in the clearance of infected B lymphocytes on B cell-associated latency [13]. Persistent infection expressing MuHV 4 antigens. The kinetics of the T/ with MHV-68 was established in mouse myeloma B CD8 cell response may be different when tested cells (NSO cells) but not in thymoma BW5147 cells [14]. against various proteins expressed during the lytic cycle Marques et al. [15] described the frequency of MHV- or those associated with latency. Thus, the cellular 68 infection in splenic B lymphocytes, in dendritic cells immune response shows a complex pattern reflecting and macrophages at acute as well as latent stages p.i. the distinct expression of virus-coded polypeptides At early intervals, B cells within the marginal zone of in antigen presenting cells (APC) and B lymphocytes germinal centres accounted for nearly the half of the [23]. The acute infectious mononucleosis (IM) like total number of infected splenocytes. syndrome shows splenomegaly, an increased number When the µMT transgenic mice (which do not of proliferating B cells and atypical mononuclear cells. produce heavy µ-chains, and therefore, do not have Thus, it represents an animal model for EBV infection mature B cells) were used to establish latency, MHV- [24]. 68 DNA persisted in the lungs, namely in pulmonary 20 J. Mistríková, J. Rajčáni 3. Comparison of biological properties had developed in a MHV-78 infected Balb/c mouse; this cell line expressed MHV antigen in a small proportion of of other MuHV 4 strains cells at passages 43-45 [34]. Usherwood et al. (1996) reported that the S11 B-lymphoma derived cell line The role for macrophages in the spread of MuHV 4 was contains MHV-68 genomes, either linear or episomal [35]. first postulated by Mistrikováet al. [25], who claimed that Tarakanova et al. (2005) found abundant positive cells adherent lung and/or peripheral blood mononuclear cells by in situ hybridization with probes specific for vtRNA in (mainly macrophages) participate in virus dissemination the samples from lymphoproliferative lesions of MHV-68 during acute infection with the MHV-72 strain. Plaque infected Balb/c mice deficient for the b2- microglobulin assay combined with nested PCR confirmed the subunit of MHC [36]. On the other hand, the frequency of hematogenic spread of MHV-72 to the mammary glands vtRNA positive cells was low in lymphomas of the same of female nu/nu Balb/c mice and its transmission to the origin and scarce in the spleen of infected animals. offspring via breast milk [26,27]. In Balb/c mice infected When athymic nude mice (BALB/c) were injected with MHV-72, the number of T/CD8 cells reached subcutaneously with MHV-72, the animals died 1 maximum by day 11 p.i., and remained elevated till month p.i.
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