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        <title>Virology Journal - Latest Articles</title>
        <link>http://www.virologyj.com</link>
        <description>The latest research articles published by Virology Journal</description>
        <dc:date>2010-03-18T00:00:00Z</dc:date>
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                                <rdf:li rdf:resource="http://www.virologyj.com/content/7/1/64" />
                                <rdf:li rdf:resource="http://www.virologyj.com/content/7/1/63" />
                                <rdf:li rdf:resource="http://www.virologyj.com/content/7/1/62" />
                                <rdf:li rdf:resource="http://www.virologyj.com/content/7/1/61" />
                                <rdf:li rdf:resource="http://www.virologyj.com/content/7/1/60" />
                                <rdf:li rdf:resource="http://www.virologyj.com/content/7/1/59" />
                                <rdf:li rdf:resource="http://www.virologyj.com/content/7/1/58" />
                                <rdf:li rdf:resource="http://www.virologyj.com/content/7/1/57" />
                                <rdf:li rdf:resource="http://www.virologyj.com/content/7/1/56" />
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        <item rdf:about="http://www.virologyj.com/content/7/1/64">
        <title>Encephalomyocarditis virus infection in an Italian zoo</title>
        <description>A fatal Encephalomyocarditis virus (EMCV) infection epidemic involving fifteen primates occurred between October 2006 and February 2007 at the Natura Viva Zoo. This large open-field zoo park located near Lake Garda in Northern Italy hosts one thousand animals belonging to one hundred and fifty different species, including various lemur species. This lemur collection is the most relevant and rich in Italy. A second outbreak between September and November 2008 involved three lemurs. In all cases, the clinical signs were sudden deaths generally without any evident symptoms or only with mild unspecific clinical signs. Gross pathologic changes were characterized by myocarditis (diffuse or focal pallor of the myocardium), pulmonary congestion, emphysema, oedema and thoracic fluid. The EMCV was isolated and recognized as the causative agent of both outbreaks. The first outbreak in particular was associated with a rodent plague, confirming that rats are an important risk factor for the occurrence of the EMCV infection.</description>
        <link>http://www.virologyj.com/content/7/1/64</link>
                <dc:creator>Elena Canelli</dc:creator>
                <dc:creator>Andrea Luppi</dc:creator>
                <dc:creator>Antonio Lavazza</dc:creator>
                <dc:creator>Davide Lelli</dc:creator>
                <dc:creator>Enrica Sozzi</dc:creator>
                <dc:creator>Ana Moreno Martin</dc:creator>
                <dc:creator>Daniela Gelmetti</dc:creator>
                <dc:creator>Ernesto Pascotto</dc:creator>
                <dc:creator>Camillo Sandri</dc:creator>
                <dc:creator>William Magnone</dc:creator>
                <dc:creator>Paolo Cordioli</dc:creator>
                <dc:source>Virology Journal 2010, 7:64</dc:source>
        <dc:date>2010-03-18T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-422X-7-64</dc:identifier>
        <prism:publicationName>Virology Journal</prism:publicationName>
        <prism:issn>1743-422X</prism:issn>
        <prism:volume>7</prism:volume>
        <prism:startingPage>64</prism:startingPage>
        <prism:publicationDate>2010-03-18T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.virologyj.com/content/7/1/63">
        <title>Nucleolar localization of influenza A NS1: striking differences between mammalian and avian cells</title>
        <description>In mammalian cells, nucleolar localization of influenza A NS1 requires the presence of a C-terminal nucleolar localization signal. This nucleolar localization signal is present only in certain strains of influenza A viruses. Therefore, only certain NS1 accumulate in the nucleolus of mammalian cells. In contrast, we show that all NS1 tested in this study accumulated in the nucleolus of avian cells even in the absence of the above described C-terminal nucleolar localization signal. Thus, nucleolar localization of NS1 in avian cells appears to rely on a different nucleolar localization signal that is more conserved among influenza virus strains.</description>
        <link>http://www.virologyj.com/content/7/1/63</link>
                <dc:creator>Romain Volmer</dc:creator>
                <dc:creator>Beryl Mazel-Sanchez</dc:creator>
                <dc:creator>Christelle Volmer</dc:creator>
                <dc:creator>Sebastien Soubies</dc:creator>
                <dc:creator>Jean-Luc Guerin</dc:creator>
                <dc:source>Virology Journal 2010, 7:63</dc:source>
        <dc:date>2010-03-17T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-422X-7-63</dc:identifier>
        <prism:publicationName>Virology Journal</prism:publicationName>
        <prism:issn>1743-422X</prism:issn>
        <prism:volume>7</prism:volume>
        <prism:startingPage>63</prism:startingPage>
        <prism:publicationDate>2010-03-17T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.virologyj.com/content/7/1/62">
        <title>Human herpesvirus-8 in northwestern China: epidemiology and characterization  among blood donors</title>
        <description>Background:
Human herpes virus 8 (HHV-8) is the etiologic agent associated with development of classical, AIDS-related, iatrogenic, and endemic Kaposi&apos;s sarcoma (KS). Several studies provide strong evidence that HHV-8 can be transmitted by blood transfusion. We evaluated the seroprevalence and potential risk factors of HHV-8 infection in blood donors in one region. We surveyed HHV-8 infection among 4461 blood donors in Xinjiang, China, a unique endemic area for HHV-8 and KS.
Results:
The HHV-8 seroprevalence was higher in local minority groups which comprise most KS cases in China, than in Han people. HHV-8 prevalence was 18.6% in the Han ethnic group, 25.9% in Uygur subjects, 29.2% in Kazak subjects, 36.8% in Mongolian subjects, and 21.9% in other ethnic groups. In several subgroups, the time of donation of whole blood seemed to be a risk factor. In HHV-8-seropositive subjects, a larger fraction of local minorities (23.9%) had high HHV-8 titers than that of Han subjects (9.2%). HHV-8 infection was associated with ethnicity and residence.
Conclusion:
HHV-8 seroprevalence was significantly high among blood donors in Xinjiang, where the prevalence of KS correlates with HHV-8 prevalence and titers in Uygur and Kazak ethnic groups. Blood exposure represented by the frequency of blood donation indicated a possible blood-borne transmission route of HHV-8 in Xinjiang. Detecting anti-HHV-8 antibodies before donation in this region is therefore important.</description>
        <link>http://www.virologyj.com/content/7/1/62</link>
                <dc:creator>Xing Wang</dc:creator>
                <dc:creator>Bin He</dc:creator>
                <dc:creator>Zhaoxia Zhang</dc:creator>
                <dc:creator>Tao Liu</dc:creator>
                <dc:creator>Hui Wang</dc:creator>
                <dc:creator>Xu Li</dc:creator>
                <dc:creator>Qiong Zhang</dc:creator>
                <dc:creator>Ke Lan</dc:creator>
                <dc:creator>Xiaomei Lu</dc:creator>
                <dc:creator>Hao Wen</dc:creator>
                <dc:source>Virology Journal 2010, 7:62</dc:source>
        <dc:date>2010-03-17T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-422X-7-62</dc:identifier>
        <prism:publicationName>Virology Journal</prism:publicationName>
        <prism:issn>1743-422X</prism:issn>
        <prism:volume>7</prism:volume>
        <prism:startingPage>62</prism:startingPage>
        <prism:publicationDate>2010-03-17T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.virologyj.com/content/7/1/61">
        <title>Efficient inhibition of hepatitis B virus replication by hepatitis delta virus ribozymes delivered by targeting retrovirus</title>
        <description>Background:
Hepatitis delta virus (HDV) ribozyme is an attractive molecular tool that can specifically recognize and catalyze the self-cleavage of the viral RNA phosphodiester backbone. However, a major obstacle in the medical application of the HDV ribozyme is the lack of specificity in the delivery of the ribozyme to defined target cells.
Results:
The objective of this study was to determine whether retroviral vectors can deliver the HDV ribozyme into the target cells and to elucidate whether HDV ribozyme plays a role in hepatitis B virus (HBV) replication. In our study, the transduction of helper-free pseudotyped retrovirus, which showed a broad host range, in human hepatoma cells was performed under 2 conditions, that is, in the presence of polymerized human serum albumin (pHSA) and in the absence of pHSA. The transduction ability in the presence of pHSA was higher than in the absence of pHSA. Moreover, HBsAg and HBeAg levels after transductions with pHSA were significantly lower than those in the absence of pHSA, thus indicating that the recombinant retrovirus had HBV-specific cleavage activity and targeted HepG2215 cells.
Conclusions:
These data suggest that this system provides a new approach for targeting hepatocytes and has a great potential in gene therapy for HBV infection.</description>
        <link>http://www.virologyj.com/content/7/1/61</link>
                <dc:creator>Chuan-Xi Wang</dc:creator>
                <dc:creator>Yan-Qin Lu</dc:creator>
                <dc:creator>Peng Qi</dc:creator>
                <dc:creator>Long-Hua Chen</dc:creator>
                <dc:creator>Jin-Xiang Han</dc:creator>
                <dc:source>Virology Journal 2010, 7:61</dc:source>
        <dc:date>2010-03-17T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-422X-7-61</dc:identifier>
        <prism:publicationName>Virology Journal</prism:publicationName>
        <prism:issn>1743-422X</prism:issn>
        <prism:volume>7</prism:volume>
        <prism:startingPage>61</prism:startingPage>
        <prism:publicationDate>2010-03-17T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.virologyj.com/content/7/1/60">
        <title>Prevalence of a virus similar to human hepatitis B virus in swine</title>
        <description>Background:
The objective of this study is to established evidence of the existence of a novel member of the hepadnavirus family endemic in swine. Temporarily this virus was designated as swine hepatitis B virus (SHBV). This SHBV can be detected by using human hepatitis B virus diagnostic kits including ELISA, immunohistochemical staining, and transmission electron microscopy (TEM). Also seroprevalence of pig farms in Beijing, China, and pathological features of SHBV infection was determined.
Results:
Screened result shows that overall prevalence of HBsAg was 24.8%, closed to that of anti-HBsAg, whereas HBeAg and anti-HBe were barely detectable. The distribution of HBsAg and HBcAg was examined by immunohistochemistry of liver samples. Typical hepatitis pathological change, such as spotty parenchymal cell degeneration, necrosis of hepatocytes and proliferation of fibrous connective tissue were observed during histopathological analysis. Analysis of HBsAg-positive serum with TEM revealed two morphologic forms, 20nm and 40nm sized particles, similar to small spherical and Danes particles of HBV. Observation of the ultrastructure of the liver also found HBV-like particles in the nucleus of hepatocytes.
Conclusion:
Our research result implies that SHBV could be a causative agent of swine. The discovery of SHBV will unveil novel evolutionary aspects of hepatitis and provides new information for further hepadnavirus research.</description>
        <link>http://www.virologyj.com/content/7/1/60</link>
                <dc:creator>Wengui Li</dc:creator>
                <dc:creator>Ruiping She</dc:creator>
                <dc:creator>Liqiang Liu</dc:creator>
                <dc:creator>Hua You</dc:creator>
                <dc:creator>Jun Yin</dc:creator>
                <dc:source>Virology Journal 2010, 7:60</dc:source>
        <dc:date>2010-03-17T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-422X-7-60</dc:identifier>
        <prism:publicationName>Virology Journal</prism:publicationName>
        <prism:issn>1743-422X</prism:issn>
        <prism:volume>7</prism:volume>
        <prism:startingPage>60</prism:startingPage>
        <prism:publicationDate>2010-03-17T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.virologyj.com/content/7/1/59">
        <title>A poxvirus Bcl-2-like gene family involved in regulation of host immune response: sequence similarity and evolutionary history</title>
        <description>Background:
Poxviruses evade the immune system of the host through the action of viral encoded inhibitors that block various signalling pathways. The exact number of viral inhibitors is not yet known. Several members of the vaccinia virus A46 and N1 families, with a Bcl-2-like structure, are involved in the regulation of the host innate immune response where they act non-redundantly at different levels of the Toll-like receptor signalling pathway. N1 also maintains an anti-apoptotic effect by acting similarly to cellular Bcl-2 proteins. Whether there are related families that could have similar functions is the main subject of this investigation.
Results:
We describe the sequence similarity existing among poxvirus A46, N1, N2 and C1 protein families, which share a common domain of approximately 110-140 amino acids at their C-termini that spans the entire N1 sequence. Secondary structure and fold recognition predictions suggest that this domain presents an all-alpha-helical fold compatible with the Bcl-2-like structures of vaccinia virus proteins N1, A52, B15 and K7. We propose that these protein families should be merged into a single one. We describe the phylogenetic distribution of this family and reconstruct its evolutionary history, which indicates an extensive gene gain in ancestral viruses and a further stabilization of its gene content.
Conclusions:
Based on the sequence/structure similarity, we propose that other members with unknown function, like vaccinia virus N2, C1, C6 and C16/B22, might have a similar role in the suppression of host immune response as A46, A52, B15 and K7, by antagonizing at different levels with the TLR signalling pathways.</description>
        <link>http://www.virologyj.com/content/7/1/59</link>
                <dc:creator>Jose Gonzalez</dc:creator>
                <dc:creator>Mariano Esteban</dc:creator>
                <dc:source>Virology Journal 2010, 7:59</dc:source>
        <dc:date>2010-03-15T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-422X-7-59</dc:identifier>
        <prism:publicationName>Virology Journal</prism:publicationName>
        <prism:issn>1743-422X</prism:issn>
        <prism:volume>7</prism:volume>
        <prism:startingPage>59</prism:startingPage>
        <prism:publicationDate>2010-03-15T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.virologyj.com/content/7/1/58">
        <title>Current antibody-based immunoassay algorithm failed to confirm three late-stage AIDS cases in China: case report</title>
        <description>Background:
Immunoassays composed of screening and confirmation are the established algorithm to confirm HIV infection in China, with a Western blot result as the final diagnosis.Case presentationIn this report, three late-stage AIDS patients were initially tested HIV antibody positive using multiple screening kits, but tested indeterminate using Western blot. HIV infection diagnosis was confirmed based on nucleic acid assays, clinic manifestations and epidemiological history. Case A was identified positive at 30 months, using Western blot, Case B at 8 months, and case C remained indeterminate until he died of Kaposi&apos;s sarcoma 4 months after HAART.
Conclusion:
The report indicates that current antibody-based testing algorithms may miss late-stage AIDS patients and therefore miss the opportunity for preventing these cases from further transmission. The report also implies that viral load assays is not easy to be universely applicated in developing country like China although it is helpful in diagnosing complicated cases of HIV infection, so the counselling before and after testing is imperative to the diagnosis of HIV infection and risk behavior survey on the eaxminee should be as detailed as possible.</description>
        <link>http://www.virologyj.com/content/7/1/58</link>
                <dc:creator>Yan Li</dc:creator>
                <dc:creator>Jin-Kou Zhao</dc:creator>
                <dc:creator>Ming Wang</dc:creator>
                <dc:creator>Zhi-Gang Han</dc:creator>
                <dc:creator>Wei-Ping Cai</dc:creator>
                <dc:creator>Bo-Jian Zheng</dc:creator>
                <dc:creator>Hui-Fang Xu</dc:creator>
                <dc:source>Virology Journal 2010, 7:58</dc:source>
        <dc:date>2010-03-15T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-422X-7-58</dc:identifier>
        <prism:publicationName>Virology Journal</prism:publicationName>
        <prism:issn>1743-422X</prism:issn>
        <prism:volume>7</prism:volume>
        <prism:startingPage>58</prism:startingPage>
        <prism:publicationDate>2010-03-15T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.virologyj.com/content/7/1/57">
        <title>Development of a new ultra sensitive real-time PCR assay (ultra sensitive RTQ-PCR) for the quantification of HBV-DNA</title>
        <description>Background:
Improved sensitivity of HBV-DNA tests is of critical importance for the management of HBV infection. Our aim was to develop and assess a new ultra sensitive in-house real-time PCR assay for HBV-DNA quantification (ultra sensitive RTQ-PCR).
Results:
Previously used HBV-DNA standards were calibrated against the WHO 1st International Standard for HBV-DNA (OptiQuant(R) HBV-DNA Quantification Panel, Accrometrix Europe B.V.). The 95% and 50% HBV-DNA detection end-point of the assay were 22.2 and 8.4 IU/mL. According to the calibration results, 1 IU/mL equals 2.8 copies/mL. Importantly the clinical performance of the ultra sensitive real-time PCR was tested similar (67%) to the Procleix Ultrio discriminatory HBV test (dHBV) (70%) in low-titer samples from patients with occult Hepatitis B. Finally, in the comparison of ultra sensitive RTQ-PCR with the commercially available COBAS TaqMan HBV Test, the in-house assay identified 94.7% of the 94 specimens as positive versus 90.4% identified by TaqMan, while the quantitative results that were positive by both assay were strongly correlated (r=0.979).
Conclusions:
We report a new ultra sensitive real time PCR molecular beacon based assay with remarkable analytical and clinical sensitivity, calibrated against the WHO 1st International standard.</description>
        <link>http://www.virologyj.com/content/7/1/57</link>
                <dc:creator>Dimitrios Paraskevis</dc:creator>
                <dc:creator>Apostolos Beloukas</dc:creator>
                <dc:creator>Catherine Haida</dc:creator>
                <dc:creator>Antigoni Katsoulidou</dc:creator>
                <dc:creator>Zisis Moschidis</dc:creator>
                <dc:creator>Helen Hatzitheodorou</dc:creator>
                <dc:creator>Agoritsa Varaklioti</dc:creator>
                <dc:creator>Vana Sypsa</dc:creator>
                <dc:creator>Angelos Hatzakis</dc:creator>
                <dc:source>Virology Journal 2010, 7:57</dc:source>
        <dc:date>2010-03-12T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-422X-7-57</dc:identifier>
        <prism:publicationName>Virology Journal</prism:publicationName>
        <prism:issn>1743-422X</prism:issn>
        <prism:volume>7</prism:volume>
        <prism:startingPage>57</prism:startingPage>
        <prism:publicationDate>2010-03-12T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.virologyj.com/content/7/1/56">
        <title>MNF, an ankyrin repeat protein of myxoma virus, is part of a native cellular SCF complex during viral infection </title>
        <description>Myxoma virus (MYXV), a member of the Poxviridae family, is the agent responsible for myxomatosis, a fatal disease in the European rabbit (Oryctolagus cuniculus). Like all poxviruses, MYXV is known for encoding multiple proteins that regulate cellular signaling pathways. Among them, four proteins share the same ANK/PRANC structure: M148R, M149R, MNF (Myxoma Nuclear factor) and M-T5, all of them described as virulence factors. This family of poxvirus proteins, recently identified, has drawn considerable attention for its potential role in modulating the host ubiquitin-proteasome system during viral infection. To date, many members of this novel protein family have been shown to interact with SCF components, in vitro. Here, we focus on MNF gene, which has been shown to express a nuclear protein presenting nine ANK repeats, one of which has been identified as a nuclear localization signal. In transfection, MNF has been shown to colocalise with the transcription factor NF-&#954;B in the nucleus of TNF&#945;-stimulated cells. Functionally, MNF is a critical virulence factor since its deletion generates an almost apathogenic virus. In this study, to pursue the investigation of proteins interacting with MNF and of its mechanism of action, we engineered a recombinant MYXV expressing a GFP-linked MNF under the control of MNF native promoter. Infection of rabbits with MYXV-GFPMNF recombinant virus provided the evidence that the GFP fusion does not disturb the main function of MNF. Hence, cells were infected with MYXV-GFPMNF and immunoprecipitation of the GFPMNF fusion protein was performed to identify MNF&apos;s partners. For the first time, endogenous components of SCF (Cullin-1 and Skp1) were co-precipitated with an ANK myxoma virus protein, expressed in an infectious context, and without over-expression of any protein.</description>
        <link>http://www.virologyj.com/content/7/1/56</link>
                <dc:creator>Sophie Blanie</dc:creator>
                <dc:creator>Jacqueline Gelfi</dc:creator>
                <dc:creator>Stephane Bertagnoli</dc:creator>
                <dc:creator>Christelle Camus-Bouclainville</dc:creator>
                <dc:source>Virology Journal 2010, 7:56</dc:source>
        <dc:date>2010-03-08T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-422X-7-56</dc:identifier>
        <prism:publicationName>Virology Journal</prism:publicationName>
        <prism:issn>1743-422X</prism:issn>
        <prism:volume>7</prism:volume>
        <prism:startingPage>56</prism:startingPage>
        <prism:publicationDate>2010-03-08T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.virologyj.com/content/7/1/55">
        <title>Decreased HIV diversity after allogeneic stem cell transplantation of an HIV-1 infected patient: a case report</title>
        <description>The human immunodeficiency virus type 1 (HIV-1) coreceptor use and viral evolution were analyzed in blood samples from an HIV-1 infected patient undergoing allogeneic stem cell transplantation (SCT). Coreceptor use was predicted in silico from sequence data obtained from the third variable loop region of the viral envelope gene with two software tools. Viral diversity and evolution was evaluated on the same samples by Bayesian inference and maximum likelihood methods. In addition, phenotypic analysis was done by comparison of viral growth in peripheral blood mononuclear cells and in a CCR5 (R5)-deficient T-cell line which was controlled by a reporter assay confirming viral tropism. In silico coreceptor predictions did not match experimental determinations that showed a consistent R5 tropism. Anti-HIV directed antibodies could be detected before and after the SCT. These preexisting antibodies did not prevent viral rebound after the interruption of antiretroviral therapy during the SCT. Eventually, transplantation and readministration of anti-retroviral drugs lead to sustained increase in CD4 counts and decreased viral load to undetectable levels. Unexpectedly, viral diversity decreased after successful SCT. Our data evidence that only R5-tropic virus was found in the patient before and after transplantation. Therefore, blocking CCR5 receptor during stem cell transplantation might have had beneficial effects and this might apply to more patients undergoing allogeneic stem cell transplantation. Furthermore, we revealed a scenario of HIV-1 dynamic different from the commonly described ones. Analysis of viral evolution shows the decrease of viral diversity even during episodes with bursts in viral load.</description>
        <link>http://www.virologyj.com/content/7/1/55</link>
                <dc:creator>Christel Kamp</dc:creator>
                <dc:creator>Timo Wolf</dc:creator>
                <dc:creator>Ignacio Bravo</dc:creator>
                <dc:creator>Benjamin Kraus</dc:creator>
                <dc:creator>Birgit Krause</dc:creator>
                <dc:creator>Britta Neumann</dc:creator>
                <dc:creator>Gudrun Winskowsky</dc:creator>
                <dc:creator>Alexander Thielen</dc:creator>
                <dc:creator>Albrecht Werner</dc:creator>
                <dc:creator>Barbara Schnierle</dc:creator>
                <dc:source>Virology Journal 2010, 7:55</dc:source>
        <dc:date>2010-03-08T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-422X-7-55</dc:identifier>
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        <prism:issn>1743-422X</prism:issn>
        <prism:volume>7</prism:volume>
        <prism:startingPage>55</prism:startingPage>
        <prism:publicationDate>2010-03-08T00:00:00Z</prism:publicationDate>
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