ABSTRACT
COVID-19 continues to exact a substantial toll on health. While mortality and morbidity associated with the pandemic are the most obvious impacts, social and economic disruptions are becoming apparent. There is reason to believe that the COVID-19 pandemic has slowed or reversed gains in clean household energy use in rural India. Here we describe phone surveys deployed repeatedly in Jharkhand and Bihar to describe pandemic-related changes in household socio-economic conditions and energy-use patterns. Over three-quarters of households reported hardships during the pandemic, including loss of employment and an inability to search for jobs. In turn, some of these households relied more on polluting fuels. Despite nearly all households preferring gas and electricity, we observed varied behaviours related to the cost of and access to these modern energy sources. We highlight the success of India's three-free-cylinders scheme, with 90% of households aware of the programme and utilizing at least one free cylinder. These findings illustrate the utility of high-frequency energy-related questionnaires and suggest that interventions to improve clean fuel accessibility and affordability can increase the resilience of transitions to clean household energy. © 2023, The Author(s).
ABSTRACT
Unlike SARS-CoV-1 and MERS-CoV, infection with SARS-CoV-2, the viral pathogen responsible for COVID-19, is often associated with neurologic symptoms that range from mild to severe, yet increasing evidence argues the virus does not ex-hibit extensive neuroinvasive properties. We demonstrate SARS-CoV-2 can infect and replicate in human iPSC-derived neurons and that infection shows limited antiviral and inflammatory responses but increased activation of EIF2 signaling following infection as determined by RNA sequencing. Intranasal infection of K18 human ACE2 transgenic mice (K18-hACE2) with SARS-CoV-2 resulted in lung pathology associated with viral replication and immune cell infiltration. In addition, similar to 50% of infected mice exhibited CNS infection characterized by wide-spread viral replication in neurons accompanied by increased expression of chemokine (Cxcl9, Cxcl10, Ccl2, Ccl5 and Ccl19) and cytokine (Ifn-lambda and Tnf-alpha) transcripts associated with microgliosis and a neuroinflammatory response consisting primarily of monocytes/macrophages. Micro-glia depletion via administration of colony-stimulating factor 1 receptor inhibitor, PLX5622, in SARS-CoV-2 infected mice did not affect survival or viral replication but did result in dampened expression of proinflammatory cytokine/chemokine transcripts and a reduction in monocyte/macrophage infiltration. These results argue that microglia are dispensable in terms of controlling SARS-CoV-2 replication in in the K18-hACE2 model but do contribute to an inflammatory response through expression of pro-inflammatory genes. Collectively, these findings contribute to previous work dem-onstrating the ability of SARS-CoV-2 to infect neurons as well as emphasizing the potential use of the K18-hACE2 model to study immunological and neuropathological aspects related to SARS-CoV-2-induced neurologic disease. IMPORTANCE Understanding the immunological mechanisms contributing to both host defense and disease following viral infection of the CNS is of critical importance given the increasing number of viruses that are capable of infecting and replicating within the nervous system. With this in mind, the present study was undertaken to evaluate the role of microglia in aiding in host defense following experimental infection of the central nervous system (CNS) of K18-hACE2 with SARS-CoV-2, the causative agent of COVID-19. Neurologic symptoms that range in severity are common in COVID-19 patients and understanding immune responses that contribute to restricting neurologic disease can provide important insight into better understanding consequences associated with SARS-CoV-2 infection of the CNS.