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The COVID-19 pandemic severely affected the medical education worldwide. The infection risk for medical students and healthcare personnel who work with COVID-19 positive cadavers or tissues remains unclear. Moreover, COVID-19 positive cadavers have been rejected by medical schools, adversely impacting the continuum of medical education. Herein, the viral genome abundance in tissues from four COVID-19 positive donors before and after embalming were compared. Tissue samples were collected from the lungs, liver, spleen, and brain both pre- and postembalming. The possible presence of infectious COVID-19 was determined by inoculating human tissue homogenates onto a monolayer of human A549-hACE2 cells and observing for cytopathic effects up to 72 h postinoculation. A real- time quantitative reverse transcription polymerase chain reaction was performed to quantify COVID-19 present in culture supernatants. Fully intact viral genome sequence was possible to obtain in samples with higher levels of virus, even several days postmortem. The embalming procedure described above substantially reduces the abundance of viable COVID-19 genomes in all tissues, sometimes even to undetectable levels. However, in some cases, COVID-19 RNA can still be detected, and a cytopathic effect can be seen both pre- and postembalmed tissues. This study suggests that embalmed COVID-19 positive cadavers might be used safely with appropriate precautions followed in gross anatomy laboratories and in clinical and scientific research. Deep lung tissue is the best specimen to test for the virus. If the tests on the lung tissues are negative, there is a very low likelihood that other tissues will show positive results.

COVID-19 remains a significant threat to public health globally. Infection in some susceptible individuals causes life-threatening acute lung injury (ALI/ARDS) and/or death. Human surfactant protein A (SP-A) is a C-type lectin expressed in the lung and other mucosal tissues, and it plays a critical role in host defense against various pathogens. The human SP-A genes ( SFTPA1 and SFTPA2 ) are highly polymorphic and comprise several common genetic variants, i.e., SP-A1 (variants 6A 2 , 6A 4 ) and SP-A2 (variants 1A 0 , 1A 3 ). Here, we elucidated the differential antiviral and immunoregulatory roles of SP-A variants in response to SARS-CoV-2 infection in vivo . Six genetically-modified mouse lines, expressing both hACE2 (SARS-CoV-2 receptor) and individual SP-A variants: (hACE2/6A 2 (6A 2 ), hACE2/6A 4 (6A 4 ), hACE2/1A 0 (1A 0 ), and hACE2/1A 3 (1A 3 ), one SP-A knockout (hACE2/SP-A KO (KO) and one hACE2/mouse SP-A (K18) mice, were challenged intranasally with 10 3 PFU SARS-CoV-2 or saline (Sham). Infected KO and 1A 0 mice had more weight loss and mortality compared to other mouse lines. Relative to other infected mouse lines, a more severe ALI was observed in KO, 1A 0 , and 6A 2 mice. Reduced viral titers were generally observed in the lungs of infected SP-A mice relative to KO mice. Transcriptomic analysis revealed an upregulation in genes that play central roles in immune responses such as MyD88 , Stat3 , IL-18 , and Jak2 in the lungs of KO and 1A 0 mice. However, Mapk1 was significantly downregulated in 6A 2 versus 1A 0 mice. Analysis of biological pathways identified those involved in lung host defense and innate immunity, including pathogen-induced cytokine, NOD1/2, and Trem1 signaling pathways. Consistent with the transcriptomic data, levels of cytokines and chemokines such as G-CSF, IL-6 and IL-1β were comparatively higher in the lungs and sera of KO and 1A 0 mice with the highest mortality rate. These findings demonstrate that human SP-A variants differentially modulate SARS-CoV-2-induced lung injury and disease severity by differentially inhibiting viral infectivity and regulating immune-related gene expressions.

Heartland virus was first isolated in 2009 from two patients in Missouri and is transmitted by the lone star tick, Amblyomma americanum. To understand disease transmission and pathogenesis, it is necessary to develop an animal model that utilizes the natural transmission route and manifests in a manner similar to documented human cases. Herein we describe our investigations on identifying A129 mice as the most appropriate small animal model for HRTV pathogenesis that mimics human clinical outcomes. We further investigated the impact of tick saliva in enhancing pathogen transmission and clinical outcomes. Our investigations revealed an increase in viral load in the groups of mice that received both virus and tick salivary gland extract (SGE). Spleens of all infected mice showed extramedullary hematopoiesis (EH), depleted white pulp, and absence of germinal centers. This observation mimics the splenomegaly observed in natural human cases. In the group that received both HRTV and tick SGE, the clinical outcome of HRTV infection was exacerbated compared to HRTV-only infection. EH scores and viral antigens in the spleen were higher in mice that received both HRTV and tick SGE. In conclusion, we have developed a small animal model that mimics natural human infection and also demonstrated the impact to tick salivary factors in exacerbating the HRTV infection.

Arthropod-borne viruses (arboviruses) have continued to emerge in recent years, posing a significant health threat to millions of people worldwide. The majority of arboviruses that are pathogenic to humans are transmitted by mosquitoes and ticks, but other types of arthropod vectors can also be involved in the transmission of these viruses. To alleviate the health burdens associated with arbovirus infections, it is necessary to focus today's research on disease control and therapeutic strategies. Animal models for arboviruses are valuable experimental tools that can shed light on the pathophysiology of infection and will enable the evaluation of future treatments and vaccine candidates. Ideally an animal model will closely mimic the disease manifestations observed in humans. In this review, we outline the currently available animal models for several viruses vectored by mosquitoes, ticks, and midges, for which there are no standardly available vaccines or therapeutics.