Co-infections and Pathogenesis of KSHV-Associated Malignancies

Thakker, Suhani; Verma, Subhash C.

doi:10.3389/fmicb.2016.00151

Cited by 36 publications

(50 citation statements)

References 169 publications

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“…KSHV participates in the progression of Kaposi's sarcoma, HIV in immune-suppressed patients, and other pathogens (Thakker and Verma, 2016). KSHV establishes lifetime persistence and exhibits two different life cycles: a prolonged latent state and a short productive or lytic life cycle.…”

Section: Exosomes In Gamma Herpesvirus Infectionmentioning

confidence: 99%

Extracellular vesicles: novel vehicles in herpesvirus infection

et al. 2017

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Herpesviruses are remarkable pathogens that have evolved multiple mechanisms to evade host immunity, ensuring their proliferation and egress. Among these mechanisms, herpesviruses utilize elaborate extracellular vesicles, including exosomes, for the intricate interplay between infected host and recipient cells. Herpesviruses incorporate genome expression products and direct cellular products into exosomal cargoes. These components alter the content and function of exosomes released from donor cells, thus affecting the downstream signalings of recipient cells. In this way, herpesviruses hijack exosomal pathways to ensure their survival and persistence, and exosomes are emerging as critical mediators for virus infection-associated intercellular communication and microenvironment alteration. In this review, the function and effects of exosomes in herpesvirus infection will be discussed, so that we will have a better understanding about the pathogenesis of herpesviruses.

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Section: Exosomes In Gamma Herpesvirus Infectionmentioning

confidence: 99%

Extracellular vesicles: novel vehicles in herpesvirus infection

et al. 2017

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“…Epstein Barr virus (EBV), the first discovered human oncovirus, is strongly associated to endemic form of Burkitt lymphoma (BL) and to several other human cancers such as nasopharyngeal carcinoma (NPC) and Hodgkin lymphoma [1][2][3]. It belongs to gammaherpesvirus family, together with Kaposi sarcoma-associated herpesvirus (KSHV), that is also linked to the pathogenesis of several human malignancies [3,4]. Besides having protumorigenic effects, both viruses interfere with the immune system cell function [5,6] and in particular of dendritic cells (DCs) [7][8][9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

EBV reduces autophagy, intracellular ROS and mitochondria to impair monocyte survival and differentiation

et al. 2018

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EBV has been reported to impair monocyte in vitro differentiation into dendritic cells (DCs) and reduce cell survival. In this study, we added another layer of knowledge to this topic and showed that these effects correlated with macroautophagy/autophagy, ROS and mitochondrial biogenesis reduction. Of note, autophagy and ROS, although strongly interconnected, have been separately reported to be induced by CSF2/GM-CSF (colony stimulating factor 2) and required for CSF2-IL4-driven monocyte in vitro differentiation into DCs. We show that EBV infects monocytes and initiates a feedback loop in which, by inhibiting autophagy, reduces ROS and through ROS reduction negatively influences autophagy. Mechanistically, autophagy reduction correlated with the downregulation of RAB7 and ATG5 expression and STAT3 activation, leading to the accumulation of SQSTM1/p62. The latter activated the SQSTM1-KEAP1-NFE2L2 axis and upregulated the anti-oxidant response, reducing ROS and further inhibiting autophagy. ROS decrease correlated also with the reduction of mitochondria, the main source of intracellular ROS, achieved by the downregulation of NRF1 and TFAM, mitochondrial biogenesis transcription factors. Interestingly, mitochondria supply membranes and ATP required for autophagy execution, thus their reduction may further reduce autophagy in EBV-infected monocytes. In conclusion, this study shows for the first time that the interconnected reduction of autophagy, intracellular ROS and mitochondria mediated by EBV switches monocyte differentiation into apoptosis, giving new insights into the mechanisms through which this virus reduces immune surveillance.

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“…Both latent and lytic cycle genes are critical for tumorigenesis and the evasion of host immune response. In addition, studies exploring co-infection and crosstalk between these viruses as well as with HIV has shown direct (virus-virus) and indirect (through host immunity) interactions, most notably affecting the transition between latent and lytic viral cycles [124,130]. …”

Section: Oral Microbiomementioning

confidence: 99%

Interplay between viruses and bacterial microbiota in cancer development

Vyshenska

Lam

Shulzhenko

et al. 2017

Seminars in Immunology

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During the last few decades we have become accustomed to the idea that viruses can cause tumors. It is much less considered and discussed, however, that most people infected with oncoviruses will never develop cancer. Therefore, the genetic and environmental factors that tip the scales from clearance of viral infection to development of cancer are currently an area of active investigation. Microbiota has recently emerged as a potentially critical factor that would affect this balance by increasing or decreasing the ability of viral infection to promote carcinogenesis. In this review, we provide a model of microbiome contribution to the development of oncogenic viral infections and viral associated cancers, give examples of this process in human tumors, and describe the challenges that prevent progress in the field as well as their potential solutions.

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Co-infections and Pathogenesis of KSHV-Associated Malignancies

Cited by 36 publications

References 169 publications

Extracellular vesicles: novel vehicles in herpesvirus infection

Extracellular vesicles: novel vehicles in herpesvirus infection

EBV reduces autophagy, intracellular ROS and mitochondria to impair monocyte survival and differentiation

Interplay between viruses and bacterial microbiota in cancer development

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