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T-cell exhaustion is defined as dysfunction of T cells during chronic virus infection or cancer (Curiel et al., 2003; Barber et al., 2006b).
Loss of CEACAM1, therefore, could result in exhausted T cells that cannot further control chronic virus infection [50].
This result reveals a novel "negative vaccination" strategy where specific CD4+ T cell unresponsiveness may be used to enhance the delayed protective antibody responses in chronic virus infections.
In aggregate, studies indicate that PD-1 expression and signaling play an important role in limiting pathogenic consequences of chronic virus infection.
We therefore decided to focus on this virus, addressing the questions of the origin of this variability and of its relation with the life style of such a chronic virus.
The presence of CXCR2 and/or signaling ligands during numerous CNS inflammatory pathologies implies a potential role for CXCR2 signaling in protection or disease progression, yet a functional role for ELR+ chemokines and/or CXCR2 in a chronic virus - induced neuroinflammatory disease remains incompletely understood.
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Ongoing immune responses hold these chronic viruses at bay while avoiding immunopathologic damage to persistently infected tissues.
Here, we summarize the parallels in immunity against HPV and other chronic viruses and discuss the general implications of our findings for the immunotherapy of chronic infections.
SOAPdenovo's performance was not markedly better at assembling acute versus chronic viruses.
We looked for presence and abundance of 9 viruses: Chronic bee paralysis virus RNA 1, Chronic bee paralysis virus RNA 2, Sacbrood virus, Deformed wing virus, Black queen cell virus, Acute bee paralysis virus, Kashmir bee virus, Varroa destructor virus 1 and Israel acute paralysis virus.
We have demonstrated an association between the epithelial injury caused by chronic herpes virus infection with the murine γ-herpes virus, MHV68, and lung fibrosis.
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