Igor Jurak
Publications
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3.04Impact points
Herpes simplex virus 1 microRNAs expressed abundantly during latent infection are not essential for latency in mouse trigeminal ganglia.
Virology. 07/2011; 417(2):239-47.
Several herpes simplex virus 1 microRNAs are encoded within or near the latency associated transcript (LAT) locus, and are expressed abundantly during latency. Some of these microRNAs can repress the expression of important viral proteins and are hypothesized to play important roles in establishing ... [more] Several herpes simplex virus 1 microRNAs are encoded within or near the latency associated transcript (LAT) locus, and are expressed abundantly during latency. Some of these microRNAs can repress the expression of important viral proteins and are hypothesized to play important roles in establishing and/or maintaining latent infections. We found that in lytically infected cells and in acutely infected mouse ganglia, expression of LAT-encoded microRNAs was weak and unaffected by a deletion that includes the LAT promoter. In mouse ganglia latently infected with wild type virus, the microRNAs accumulated to high levels, but deletions of the LAT promoter markedly reduced expression of LAT-encoded microRNAs and also miR-H6, which is encoded upstream of LAT and can repress expression of ICP4. Because these LAT deletion mutants establish and maintain latent infections, these microRNAs are not essential for latency, at least in mouse trigeminal ganglia, but may help promote it.
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4.66Impact points
Mammalian alphaherpesvirus miRNAs.
Biochimica et biophysica acta. 06/2011; 1809(11-12):641-53.
Mammalian alphaherpesviruses are major causes of human and veterinary disease. During productive infection, these viruses exhibit complex and robust patterns of gene expression. These viruses also form latent infections in neurons of sensory ganglia in which productive cycle gene expression is highl... [more] Mammalian alphaherpesviruses are major causes of human and veterinary disease. During productive infection, these viruses exhibit complex and robust patterns of gene expression. These viruses also form latent infections in neurons of sensory ganglia in which productive cycle gene expression is highly repressed. Both modes of infection provide advantageous opportunities for regulation by microRNAs. Thus far, published data regarding microRNAs are available for six mammalian alphaherpesviruses. No microRNAs have yet been detected from varicella zoster virus. The five other viruses-herpes simplex viruses-1 and -2, herpes B virus, bovine herpesvirus-1, and pseudorabies virus-representing both genera of mammalian alphaherpesviruses have been shown to express microRNAs. In this article, we discuss these microRNAs in terms of where they are encoded in the viral genome relative to other viral transcripts; whether they are expressed during productive or latent infection; their potential targets; what little is known about their actual targets and functions during viral infection; and what little is known about the interactions of these viruses with the host microRNA machinery. This article is part of a Special Issue entitled: "MicroRNAs in viral gene regulation".
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5.15Impact points
Mutations in the M112/M113-coding region facilitate murine cytomegalovirus replication in human cells.
Journal of virology. 08/2010; 84(16):7994-8006.
Cytomegaloviruses, representatives of the Betaherpesvirinae, cause opportunistic infections in immunocompromised hosts. They infect various cells and tissues in their natural host but are highly species specific. For instance, human cytomegalovirus (HCMV) does not replicate in mouse cells, and human... [more] Cytomegaloviruses, representatives of the Betaherpesvirinae, cause opportunistic infections in immunocompromised hosts. They infect various cells and tissues in their natural host but are highly species specific. For instance, human cytomegalovirus (HCMV) does not replicate in mouse cells, and human cells are not permissive for murine cytomegalovirus (MCMV) infection. However, the underlying molecular mechanisms are so far poorly understood. In the present study we isolated and characterized a spontaneously occurring MCMV mutant that has gained the capacity to replicate rapidly and to high titers in human cells. Compared to the parental wild-type (wt) virus, this mutant formed larger nuclear replication compartments and replicated viral DNA more efficiently. It also disrupted promyelocytic leukemia (PML) protein nuclear domains with greater efficiency but caused less apoptosis than did wt MCMV. Sequence analysis of the mutant virus genome revealed mutations in the M112/M113-coding region. This region is homologous to the HCMV UL112-113 region and encodes the viral early 1 (E1) proteins, which are known to play an important role in viral DNA replication. By introducing the M112/M113 mutations into wt MCMV, we demonstrated that they are sufficient to facilitate MCMV replication in human cells and are, at least in part, responsible for the efficient replication capability of the spontaneously adapted virus. However, additional mutations probably contribute as well. These results reveal a previously unrecognized role of the viral E1 proteins in regulating viral replication in different cells and provide new insights into the mechanisms of the species specificity of cytomegaloviruses.
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5.15Impact points
Numerous conserved and divergent microRNAs expressed by herpes simplex viruses 1 and 2.
Journal of virology. 02/2010; 84(9):4659-72.
Certain viruses use microRNAs (miRNAs) to regulate the expression of their own genes, host genes, or both. Previous studies have identified a limited number of miRNAs expressed by herpes simplex viruses 1 and 2 (HSV-1 and -2), some of which are conserved between these two viruses. To more comprehens... [more] Certain viruses use microRNAs (miRNAs) to regulate the expression of their own genes, host genes, or both. Previous studies have identified a limited number of miRNAs expressed by herpes simplex viruses 1 and 2 (HSV-1 and -2), some of which are conserved between these two viruses. To more comprehensively analyze the miRNAs expressed by HSV-1 or HSV-2 during productive and latent infection, we applied a massively parallel sequencing approach. We were able to identify 16 and 17 miRNAs expressed by HSV-1 and HSV-2, respectively, including all previously known species, and a number of previously unidentified virus-encoded miRNAs. The genomic positions of most miRNAs encoded by these two viruses are within or proximal to the latency-associated transcript region. Nine miRNAs are conserved in position and/or sequence, particularly in the seed region, between these two viruses. Interestingly, we did not detect an HSV-2 miRNA homolog of HSV-1 miR-H1, which is highly expressed during productive infection, but we did detect abundant expression of miR-H6, whose seed region is conserved with HSV-1 miR-H1 and might represent a functional analog. We also identified a highly conserved miRNA family arising from the viral origins of replication. In addition, we detected several pairs of complementary miRNAs and we found miRNA-offset RNAs (moRs) arising from the precursors of HSV-1 and HSV-2 miR-H6 and HSV-2 miR-H4. Our results reveal elements of miRNA conservation and divergence that should aid in identifying miRNA functions.
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9.43Impact points
Human papillomavirus 16 E7 inactivator of retinoblastoma family proteins complements human cytomegalovirus lacking UL97 protein kinase.
Proceedings of the National Academy of Sciences of the United States of America. 09/2009; 106(39):16823-8.
Several different families of DNA viruses encode proteins that inactivate the cellular retinoblastoma tumor suppressor protein (pRb), which normally functions to bind E2F transcription factors and restrict expression of genes necessary for cellular processes including DNA replication. Human cytomega... [more] Several different families of DNA viruses encode proteins that inactivate the cellular retinoblastoma tumor suppressor protein (pRb), which normally functions to bind E2F transcription factors and restrict expression of genes necessary for cellular processes including DNA replication. Human cytomegalovirus (HCMV) UL97, a protein kinase functionally orthologous to cellular cyclin-dependent kinases, phosphorylates pRb on inactivating residues during HCMV infection. To assess if such phosphorylation is biologically relevant, we tested whether the human papillomavirus type 16 E7 protein, which inactivates pRb family proteins by direct binding and destabilization, could substitute for UL97 during HCMV infection. In the absence of UL97, expression of wild-type E7 protein, but not a mutant E7 unable to bind pRb family proteins, restored E2F-responsive cellular gene expression, late viral gene expression, and viral DNA synthesis to levels normally observed during wild-type virus infection of quiescent cells. UL97-null mutants exhibited more pronounced defects in virus production and DNA synthesis in quiescent cells as compared to serum-fed, cycling cells. E7 expression substantially enhanced infectious virus production in quiescent cells, but did not complement the defects observed during UL97-null virus infection of cycling cells. Thus, a primary role of UL97 is to inactivate pRb family proteins during infection of quiescent cells, and this inactivation likely abets virus replication by induction of cellular E2F-responsive genes. Our findings have implications for human cytomegalovirus disease and for drugs that target UL97.
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34.48Impact points
MicroRNAs expressed by herpes simplex virus 1 during latent infection regulate viral mRNAs.
Nature. 08/2008;
Herpesviruses are characterized by their ability to maintain life-long latent infections in their animal hosts. However, the mechanisms that allow establishment and maintenance of the latent state remain poorly understood. Herpes simplex virus 1 (HSV-1) establishes latency in neurons of sensory gang... [more] Herpesviruses are characterized by their ability to maintain life-long latent infections in their animal hosts. However, the mechanisms that allow establishment and maintenance of the latent state remain poorly understood. Herpes simplex virus 1 (HSV-1) establishes latency in neurons of sensory ganglia, where the only abundant viral gene product is a non-coding RNA, the latency associated transcript (LAT). Here we show that LAT functions as a primary microRNA (miRNA) precursor that encodes four distinct miRNAs in HSV-1 infected cells. One of these miRNAs, miR-H2-3p, is transcribed in an antisense orientation to ICP0-a viral immediate-early transcriptional activator that is important for productive HSV-1 replication and thought to have a role in reactivation from latency. We show that miR-H2-3p is able to reduce ICP0 protein expression, but does not significantly affect ICP0 messenger RNA levels. We also identified a fifth HSV-1 miRNA in latently infected trigeminal ganglia, miR-H6, which derives from a previously unknown transcript distinct from LAT. miR-H6 shows extended seed complementarity to the mRNA encoding a second HSV-1 transcription factor, ICP4, and inhibits expression of ICP4, which is required for expression of most HSV-1 genes during productive infection. These results may explain the reported ability of LAT to promote latency. Thus, HSV-1 expresses at least two primary miRNA precursors in latently infected neurons that may facilitate the establishment and maintenance of viral latency by post-transcriptionally regulating viral gene expression.
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5.15Impact points
Murine cytomegalovirus m38.5 protein inhibits Bax-mediated cell death.
Journal of virology. 06/2008; 82(10):4812-22.
Many viruses encode proteins that inhibit the induction of programmed cell death at the mitochondrial checkpoint. Murine cytomegalovirus (MCMV) encodes the m38.5 protein, which localizes to mitochondria and protects human HeLa cells and fibroblasts from apoptosis triggered by proteasome inhibitors b... [more] Many viruses encode proteins that inhibit the induction of programmed cell death at the mitochondrial checkpoint. Murine cytomegalovirus (MCMV) encodes the m38.5 protein, which localizes to mitochondria and protects human HeLa cells and fibroblasts from apoptosis triggered by proteasome inhibitors but not from Fas-induced apoptosis. However, the ability of this protein to suppress the apoptosis of murine cells and its role during MCMV infection have not been investigated previously. Here we show that m38.5 is expressed at early time points during MCMV infection. Cells infected with MCMVs lacking m38.5 showed increased sensitivity to cell death induced by staurosporine, MG132, or the viral infection itself compared to the sensitivity of cells infected with wild-type MCMV. This defect was eliminated when an m38.5 or Bcl-X(L) gene was inserted into the genome of a deletion mutant. Using fibroblasts deficient in the proapoptotic Bcl-2 family proteins Bak and/or Bax, we further demonstrated that m38.5 protected from Bax- but not Bak-mediated apoptosis and interacted with Bax in infected cells. These results consolidate the role of m38.5 as a viral mitochondrion-localized inhibitor of apoptosis and its functional similarity to the human cytomegalovirus UL37x1 gene product. Although the m38.5 gene is not homologous to the UL37x1 gene at the sequence level, m38.5 is conserved among rodent cytomegaloviruses. Moreover, the fact that MCMV-infected cells are protected from both Bak- and Bax-mediated cell death suggests that MCMV possesses an additional, as-yet-unidentified mechanism to block Bak-mediated apoptosis.
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5.16Impact points
A single mutation at Tyr143 of human S-adenosylhomocysteine hydrolase renders the enzyme thermosensitive and affects the oxidation state of bound cofactor nicotinamide-adenine dinucleotide.
The Biochemical journal. 01/2007; 400(2):245-53.
Recently, we have described the first human case of AdoHcyase (S-adenosylhomocysteine hydrolase) deficiency. Two point mutations in the AdoHcyase gene, the missense mutation p.Y143C (AdoHcyase in which Tyr143 is replaced by cysteine) and the truncation mutation p.W112stop (AdoHcyase in which Trp112 ... [more] Recently, we have described the first human case of AdoHcyase (S-adenosylhomocysteine hydrolase) deficiency. Two point mutations in the AdoHcyase gene, the missense mutation p.Y143C (AdoHcyase in which Tyr143 is replaced by cysteine) and the truncation mutation p.W112stop (AdoHcyase in which Trp112 is replaced by opal stop codon) were identified [Barić, Fumić, Glenn, Cuk, Schulze, Finkelstein, James, Mejaski-Bosnjak, Pazanin, Pogribny et al. (2004) Proc. Natl. Acad. Sci. U.S.A. 101, 4234-4239]. To elucidate the molecular and catalytic properties of AdoHcyase, we have made recombinant wild-type and mutant p.Y143C (AdoHcyase in which Tyr143 is replaced by cysteine) enzymes for a comparative analysis. The catalytic rates of p.Y143C protein in the directions of S-adenosylhomocysteine synthesis or hydrolysis are decreased from 65% to 75%. Further, the oxidation states of coenzyme NAD differ between mutant and wild-type protein, with an increased NADH accumulation in the mutant p.Y143C enzyme of 88% NADH (wild-type contains 18% NADH). Quantitative binding of NAD is not affected. Native polyacrylamide gel electrophoresis showed, that mutant p.Y143C subunits are able to form the tetrameric complex as is the wild-type enzyme. CD analysis showed that the p.Y143C mutation renders the recombinant protein thermosensitive, with an unfolding temperature significantly reduced by 7 degrees C compared with wild-type protein. Change of Glu115 to lysine in wild-type protein causes a change in thermosensitivity almost identical with that found in the p.Y143C enzyme, indicating that the thermosensitivity is due to a missing hydrogen bond between Tyr143 and Glu115. We emphasize involvement of this particular hydrogen bond for subunit folding and/or holoenyzme stability. In summary, a single mutation in the AdoHcyase affecting both the oxidation state of bound co-factor NAD and enzyme stability is present in a human with AdoHcyase deficiency.
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8.99Impact points
Induction of apoptosis limits cytomegalovirus cross-species infection.
The EMBO journal. 07/2006; 25(11):2634-42.
Cross-species infections are responsible for the majority of emerging and re-emerging viral diseases. However, little is known about the mechanisms that restrict viruses to a certain host species, and the factors viruses need to cross the species barrier and replicate in a different host. Cytomegalo... [more] Cross-species infections are responsible for the majority of emerging and re-emerging viral diseases. However, little is known about the mechanisms that restrict viruses to a certain host species, and the factors viruses need to cross the species barrier and replicate in a different host. Cytomegaloviruses (CMVs) are representatives of the beta-herpesviruses that are highly species specific. They replicate only in cells of their own or a closely related species. In this study, the molecular mechanism underlying the cytomegalovirus species specificity was investigated. We show that infection of human cells with the murine cytomegalovirus (MCMV) triggers the intrinsic apoptosis pathway involving caspase-9 activation. MCMV can break the species barrier and replicate in human cells if apoptosis is blocked by Bcl-2 or a functionally analogous protein. A single gene of the human cytomegalovirus encoding a mitochondrial inhibitor of apoptosis is sufficient to allow MCMV replication in human cells. Moreover, the same principle facilitates replication of the rat cytomegalovirus in human cells. Thus, induction of apoptosis serves as an innate immune defense to inhibit cross-species infections of rodent CMVs.
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2.14Impact points
Helicobacter pylori colonization of tongue mucosa--increased incidence in atrophic glossitis and burning mouth syndrome (BMS).
Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology. 11/2001; 30(9):560-3.
Nested polymerase chain reaction (PCR) was performed to detect the presence of Helicobacter pylori in tongue mucosa in 268 patients divided into four groups according to their diagnosis: 87 with atrophic glossitis, 37 with benign migratory glossitis and 144 with burning mouth syndrome (BMS). The lat... [more] Nested polymerase chain reaction (PCR) was performed to detect the presence of Helicobacter pylori in tongue mucosa in 268 patients divided into four groups according to their diagnosis: 87 with atrophic glossitis, 37 with benign migratory glossitis and 144 with burning mouth syndrome (BMS). The latter group was subdivided according to anatomic site of burning sensation: subgroup A (54 patients) with complaints limited to tongue and subgroup B (90 patients) with burning sensations in other parts of oral mucosa. H. pylori was found in 43 samples (16%). Bacteria were significantly less present in tongue mucosa affected with benign migratory glossitis compared with atrophic glossitis and BMS (P=0.025). This difference was more obvious when compared with atrophic glossitis only (P=0.006). Mucosal changes in these conditions might make the oral environment more acceptable for H. pylori colonization compared with normal mucosa, and this mechanism may play a role in its oro-oral transmission.
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2.14Impact points
Helicobacter pylori in oral aphthous ulcers.
Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology. 12/2000; 29(10):523-5.
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Učinak struganja i poliranja korijena na kliničke i mikrobioloπke čimbenike parodontnih bolesti
Acta stomatologica Croatica (ascro-editor@sfzg.hr); Vol.35 No.1.
The occurence of periodontal pathogens in subgingival flora in periodontitis is a risk for periodontal disease progression. Therefore microbiologic diagnostic procedures are justifiably indicated in the detection of pathogens, monitoring of therapy success and outcome of the disease. The aim of this... [more] The occurence of periodontal pathogens in subgingival flora in periodontitis is a risk for periodontal disease progression. Therefore microbiologic diagnostic procedures are justifiably indicated in the detection of pathogens, monitoring of therapy success and outcome of the disease. The aim of this study was to show the effect of scaling and root planing on clinical and microbiological factors in 28 patients with chronic and aggressive periodontitis. Clinical assessment and microbiological testing were performed prior to, and three months after mechanical therapy. The presence or absence of bacterial plaque, gingival bleeding, pocket depth and attachment loss were assessed before and three months after scaling and root planing. Samples of subgingival plaque taken from periodontal pockets, were analysed by polymerase chain reaction technique for the presence of seven bacterial pathogens. Results of clinical parameters and bacterial prevalence were analysed before and after therapy by Wilcoxon Rank test. The mean pocket depth significantly decreased from 3.9 to 3.0 mm. Clinical attachment level decreased moderately from 4.1 to 3.8 mm. Mean plaque and gingival bleeding values also decreased after therapy. The prevalence of subgingival pathogens in relation to subjects was as follows: only one pathogenic species was found in 28.6%, two were found in 46.4% and three in 14.3% of subjects. The most prevalent pathogens were bacteroides forsythus in 85.7%, Porphyromonas gingivalis in 32.1%, Actinobacillus actinomycetemcomitans and Fusobacterium in 32.1% of subjects. After therapy the prevalence of pathogens decreased moderately. The total number of tested pathogens decreased in 12 subjects and this result was statistically significant. (p=0.001). In 16 subjects the number of pathogens was the same, and did not increase in any of the subjects. The results indicate that the effect of scaling and root planing in the treatment of periodontitis was effective in achieving clinical and microbiological improvement by decreasing the prevalence of pathogens responsible for disease progression.
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The molecular mechanism of the Cytomegalovirus species specificity
Viruses have undergone a coevolution with their hosts, resulting in a specific adaptation to them. Consequently, many viruses have a limited host range. Occasionally, viruses acquire an adaptive mutation, which allows infection and replication in a different species as shown recently for the human i... [more] Viruses have undergone a coevolution with their hosts, resulting in a specific adaptation to them. Consequently, many viruses have a limited host range. Occasionally, viruses acquire an adaptive mutation, which allows infection and replication in a different species as shown recently for the human immunodeficiency virus and influenza virus. Cross-species infections are responsible for the majority of emerging and re-emerging viral diseases. However, little is known about the mechanisms that restrict viruses to a certain host species, and the factors viruses need to cross the species barrier and replicate in a different host. Cytomegaloviruses are prototypes of the beta-herpesvirus subfamily and are highly species specific. They replicate only in cells of their own or a closely related species. The molecular mechanism underlying their species specificity is poorly understood and was investigated in this study. An initial observation showed that murine cytomegalovirus (MCMV) can replicate in human 293 and 911 cells, but not in any other human cells tested. Both cell lines are transformed with adenoviral E1 genes that encode a transcriptional transactivator (E1A) and two suppressors of apoptosis (E1B-55k and E1B-19k). This has led to the hypothesis that these functions are required for MCMV replication in human cells. Further analysis revealed that normal human cells died rapidly after infection of caspase-9-mediated apoptosis. Apoptosis induced by MCMV can be suppressed by broad-spectrum caspase inhibitors, and virus replication can be rescued, indicating a major role of caspases in this process. Furthermore, over-expression of a mitochondria-localized inhibitor of apoptosis, a Bcl-2-like protein, prevented apoptosis induced by this virus. Human cells resistant to apoptosis allowed also an efficient MCMV replication. The important role of Bcl-2-like proteins for cytomegalovirus cross-species infections was subsequently confirmed by inserting the corresponding genes, and other inhibitors of apoptosis and control genes into the MCMV genome. Only recombinant viruses expressing a Bcl-2-like protein were able to replicate in human cells. A single gene of human cytomegalovirus encoding a mitochondrial inhibitor of apoptosis was sufficient to allow MCMV replication in human cells. Moreover, the same principle facilitated replication of the rat cytomegalovirus in human cells. Thus, induction of apoptosis limits rodent cytomegalovirus cross-species infection. Viren durchliefen eine gemeinsame Evolution mit ihren Wirtsorganismen, die zu einer spezifischen Anpassung der Viren an ihren jeweiligen Wirt führte. Als Folge dessen verfügen viele Viren über ein eng begrenztes Wirtsspektrum. Gelegentlich machen Viren Veränderungen durch, die es ihnen erlauben, einen neuen Wirt zu infizieren und in ihm zu replizieren, wie dies in jüngster Vergangenheit beim humanen Immundefizienz-Virus oder beim Grippevirus geschehen ist. Spezies-übergreifende Infektionen sind für die meisten neuen und wiederauftauchenden Viruserkrankungen verantwortlich. Allerdings ist bisher wenig über die Mechanismen bekannt, die Viren auf einen bestimmten Wirt beschränken, und welche Faktoren Viren zur Überwindung der Spezies-Barriere und zur Vermehrung in einer neuen Wirtsspezies benötigen. Cytomegaloviren sind Prototypen der beta-Herpesvirus Unterfamilie und verfügen über eine ausgeprägte Spezies-Spezifität. Sie vermehren sich nur in Zellen der eigenen oder einer eng verwandten Wirtsspezies. Der molekulare Mechanismus, der dieser Spezies-Spezifität zugrunde liegt, ist noch weitgehend unbekannt und stellt deshalb das Thema dieser Arbeit dar. Initiale Beobachtungen zeigten, dass sich das Maus-Cytomegalovirus (MCMV) ausschließlich in menschlichen 293 und 911 Zellen, aber keiner anderen getesteten menschlichen Zelle vermehren ließ. Diese beiden Zelllinien sind mit Adenovirus E1-Genen transformiert, die den Transkriptions-Transaktivator E1A sowie zwei Apoptose-Inhibitoren (E1B-55k und E1B-19k) kodieren. Daher lag die Hypothese nahe, dass diese Funktionen benötigt werden, um eine MCMV-Replikation in menschlichen Zellen zu ermöglichen. Außerdem konnte gezeigt werden, dass normale menschliche Zellen nach Infektion rapide absterben, und zwar durch eine Caspase-9-vermittelte Apoptose. Die Induktion der Apoptose durch MCMV lässt sich durch Caspase-Inhibitoren unterdrücken, wodurch die virale Replikation wiederhergestellt wird. Dies deutet auf eine Schlüsselfunktion der Caspasen für diesen Prozess hin. Durch Überexpression eines mitochondrialen Apoptose-Inhibitors, d.h. eines Bcl-2-ähnlichen Proteins, in menschlichen Zellen ließ sich die Virus-induzierte Apoptose verhindern. Diese Zellen erlaubten ebenfalls eine effiziente MCMV-Replikation. Die Bedeutung Bcl-2-ähnlicher Proteine für die Spezies-übergreifende Cytomegalovirus-Infektion wurde sowohl durch die Integration korrespondierender Gene, alsauch durch die Integration anderer Inhibitioren der Apoptose oder von Kontroll-Genen in das MCMV Genom bestätigt. Nur rekombinante Viren, die ein Bcl-2-ähnliches Protein kodieren, konnten in menschlichen Zellen vermehrt werden. Ein einziges Gen des humanen Cytomegalovirus, das einen mitochondrialen Apoptose-Inhibitor kodiert, reichte aus, um eine MCMV-Replikation in menschlichen Zellen zu ermöglichen. Zusätzlich konnte gezeigt werden, dass dieselben Prinzipien für eine Replikation des Ratten-Cytomegalovirus in menschlichen Zellen gelten. Zusammenfassend kann festgestellt werden, dass die Induktion der Apoptose eine Spezies-übergreifende Infektion bei den Nagetier-Cytomegaloviren einschränkt.
Following (4)
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Michael Nevels
Universität Regensburg -
Wolfram Brune
HPI Hamburg -
Luka Cicin-Sain
Helmholtz-Zentrum für Infektionsforschung -
Jeremy P Kamil
LSU Health Sciences Center - Shreveport
