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Soma, P. S.

Publications and source records attributed to Soma, P. S..

3 recordsLinked to original sources

Pathogenesis and host response to a novel Tacaribe virus isolate in experimentally-infected Jamaican fruit bats

Tacaribe virus (TCRV) was the first arenavirus discovered in the New World and was isolated from Artibeus bats in Trinidad and Tobago in the 1950s. One isolate, TRVL-11573, remains but it was passaged by intracranial inoculation of newborn mice 22 times that likely changed its biology. This isolate has been extensively used for arenavirus research, including our previous work that showed it can cause fatal neurological disease in Jamaican fruit bats (Artibeus jamaicensis). Another divergent TCRV, DOM2014, was recently identified in transcriptome data from a Jamaican fruit bat captured in the Dominican Republic that contained TCRV genome. A kidney fragment homogenate from this bat was inoculated into Jamaican fruit bats and all became infected with signs of mild liver disease. Experimental challenge of Jamaican fruit bats with DOM2014 led to nonfatal infection that persisted through the end of the study on day 21 and with contact transmission to naive bats. Histopathology, immunohistochemistry and serum chemistry confirmed infection and mild liver disease, but none of the bats produced neutralizing antibodies. B cell receptor transcripts suggested limited somatic hypermutation that could explain the lack of detectable neutralizing antibodies. Transcriptome profiling of livers and spleens showed signatures of a typical innate antiviral response; however, evidence of adaptive immune suppression was also present. Similarly, liver transcriptome analysis showed signatures of an expected innate antiviral response and metabolic dysfunction. The isolation of TCRV DOM2014 provides a relevant model for the study of a bat reservoir host, and which may challenge the extensive work previously conducted with TRVL-11573. IMPORTANCESeveral New World arenaviruses cause disease in humans and many are BSL-4 agents. TCRV strain TRVL-11573 has been used since the 1950s to study arenavirus biology; however, because it was intracranially passaged in newborn mice and Vero cells, it likely accumulated mutations that changed its biology. This assertion has been reinforced in recent years with discovery of divergent TCRV sequences in wild Artibeus bats that are substantially different than TRVL-11573, thus the prototype strain is unlikely to represent wildtype TCRV. The isolation of a new TCRV strain that has retained its genome fidelity allows a better understanding of TCRVs biology and pathogenic potential. The availability of pathogen-free Jamaican fruit bats and cell lines that are permissive for TCRV DOM2014 will also help retain the biological features of the virus. Collectively, this is among the most tractable bat reservoir host models developed and provides a system for dissection of how bats host viruses. Moreover, it may be a suitable model for the study of therapeutics and vaccines for New World arenaviruses.

microbiology↗

Perturbed pediatric serum metabolome in mild and severe dengue disease

Dengue viruses (DENVs) are the most prevalent arboviruses affecting humans. Four billion people are at risk of infection and this burden is rapidly increasing due to geographic expansion of the mosquito vector. Infection with any of the four serotypes of DENV can result in a self-limiting disease but debilitating febrile illness (DF), and some infections progress to severe disease with manifestations such as hemorrhage and shock. DENV infection drives the metabolic state of host cells for viral benefit and induces a host-immune response that has metabolic implications that link to disease. In this study, a dynamic metabolic response to DENV infection and disease was measured in 535 pediatric patient sera using liquid chromatography-mass spectrometry. The metabolome was interrogated to discover biochemical pathways and identify key metabolites perturbed in severe dengue disease. A biomarker panel of thirty-two perturbed metabolites was utilized to classify DF, and severe dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS) with high sensitivity and specificity equating to a balanced accuracy of 96.9%. Some metabolites that were structurally confirmed here belong to important biochemical pathways of omega-3 and omega-6 fatty acids, sphingolipids, purines, and tryptophan metabolism. A previously reported trend between serotonin and platelets in DHF patients has been expanded upon here to reveal a major depletion of serotonin, but not platelets, in DSS patients. This study differentiated and classified DF and DHF/DSS using a serum metabolic biomarker panel based on perturbed biochemical pathways that have potential implications for severe dengue disease. One sentence summary: Metabolic biomarkers distinguish dengue hemorrhagic fever and dengue shock syndrome from dengue fever and lend insight to severe disease pathology

systems biology↗

Acyl-CoA Thioesterases; a rheostat that controls activated fatty acids modulates dengue virus serotype 2 replication

During infection with dengue viruses (DENVs), the lipid landscape within host cells is significantly altered to assemble membrane platforms that support viral replication and particle assembly. Fatty acyl-CoAs are key intermediates in the biosynthesis of complex lipids that form these membranes. They also function as key signaling lipids in the cell. Here, we carried out loss of function studies on acyl-CoA thioesterases (ACOTs), a family of enzymes that hydrolyze fatty acyl-CoAs to free fatty acids and coenzyme A, to understand their influence on the lifecycle of DENVs. Loss of function of the type I ACOTs 1 (cytoplasmic) and 2 (mitochondrial) together significantly increased DENV serotype 2 (DENV2) viral replication and infectious particle release. However, isolated knockdown of mitochondrial ACOT2 significantly decreased DENV2 protein translation, genome replication, and infectious virus release. Furthermore, loss of ACOT7 function, a mitochondrial type II ACOT, similarly suppressed DENV2. As ACOT1 and ACOT2 are splice variants, these data suggest that location (cytosol and mitochondria, respectively) rather than function of these proteins may account for the differences in DENV2 infection phenotype. Additionally, loss of mitochondrial ACOT2 and ACOT7 expression also altered the expression of several ACOTs located in multiple organelle compartments within the cell highlighting a complex relationship between ACOTs in the DENV2 virus lifecycle.

microbiology↗