Estimating China's CO2 emissions under the influence of COVID-19 epidemic using a novel fractional multivariate nonlinear grey model

The COVID-19 pandemic has posed a severe challenge to the global economic recovery and China's economic growth. Although China has achieved stage victory against the epidemic, the impact and influence of the epidemic on China's economy will linger. On the positive side, the epidemic has led to a dramatic reduction in air pollution levels and a sharp slowdown in greenhouse gas emissions such as CO2. Forecasting China's CO2 emissions under the impact of the COVID-19 epidemic is crucial for formulating policies that contribute to smooth economic development and rational energy consumption. To this end, this paper improves on the traditional grey model, GM(1, N), by developing a novel fractional multivariate nonlinear grey model, FMNGM(q, N). These improvements include two key points. First, different power exponents are assigned to each relevant factor variable to explain their nonlinear, uncertain, and complicated relationships with the system characteristic variables. Second, the integer accumulation is changed to fractional accumulation to preprocess the data, and the Caputo-type fractional derivative is used to characterize the endogenous relationships among the system characteristic data. In addition, the quantum particle swarm optimization (QPSO) algorithm is used to optimize the above parameters with the goal of minimizing MAPE. The collected data on China's CO2 emission from 2001 to 2018 were divided into two parts according to different stages of economic development: 2001–2009 and 2010–2018. Both sets of data were modelled and analysed separately and compared with other models. Results showed that the proposed model had better prediction accuracy than other models. Finally, the model built using the 2010–2018 data was used to forecast China's CO2 emissions. Results show that China's CO2 emissions in 2020 under the impact of COVID-19 will decrease by approximately 3.15% from 2019 to 9893 million tons. The results bear important policy implications for planners in investment in clean energy and infrastructure to achieving the goal of a low-carbon transition.

Understanding Stereotypes of Chinese International Students in a U.S. University: A Case Study

The recent coronavirus pandemic, combined with Trump's anti-China rhetoric, made the international students and scholars of Chinese origin the easy racist target. A qualitative case study with 34 undergraduate Chinese international students (CIS) and 10 of their chosen faculty members, the study examined CISs studying abroad experiences in a U.S. university before, during and after the pandemic. Guided by the frameworks of neo-racism and model minority stereotype, this study showed that before the pandemic, there was implicit racism directed toward CIS in the academia while explicit racist attack was evident during and after the outbreak of the pandemic. Practical applications were discussed focusing on how the U.S. higher educational institutes could create a more inclusive environment for the CIS and the other international students.

Emerging SARS-CoV-2 variants expand species tropism to rodents (preprint)

Mice are not susceptible to wildtype SARS-CoV-2 infection. Emerging SARS-CoV-2 variants including B.1.1.7, B.1.351, P.1, and P.3 contain mutations in spike, which have been suggested to associate with an increased recognition of mouse ACE2, raising the postulation that they may have evolved to expand species tropism to rodents. Here, we investigated the capacity of B.1.1.7 and other emerging SARS-CoV-2 variants in infecting mouse (Mus musculus) and rats (Rattus norvegicus) under in vitro and in vivo settings. Our results show that B.1.1.7 and P.3, but not B.1 or wildtype SARS-CoV-2, can utilize mouse and rat ACE2 for virus entry in vitro. High infectious virus titers, abundant viral antigen expression, and pathological changes are detected in the nasal turbinate and lung of B.1.1.7-inocluated mice and rats. Together, these results reveal that the current predominant circulating SARS-CoV-2 variant, B.1.1.7, has gained the capability to expand species tropism to rodents.

A molecularly engineered, broad-spectrum anti-coronavirus lectin inhibits SARS-CoV-2 and MERS-CoV infection in vivo (preprint)

Coronaviruses have repeatedly crossed species barriers to cause epidemics1. “Pan-coronavirus” antivirals targeting conserved viral components involved in coronavirus replication, such as the extensively glycosylated spike protein, can be designed. Here we show that the rationally engineered H84T-banana lectin (H84T-BanLec), which specifically recognizes high-mannose found on viral proteins but seldom on healthy human cells2, potently inhibits the highly virulent MERS-CoV, pandemic SARS-CoV-2 and its variants, and other human-pathogenic coronaviruses at nanomolar concentrations. MERS-CoV-infected human DPP4-transgenic mice treated by H84T-BanLec have significantly higher survival, lower viral burden, and reduced pulmonary damage. Similarly, prophylactic or therapeutic H84T-BanLec is effective against SARS-CoV-2 in hamsters. Importantly, intranasally and intraperitoneally administered H84T-BanLec are comparably effective. Time-of-drug-addition assay shows that H84T-BanLec targets virus entry. Real-time structural analysis with high-speed atomic force microscopy depicts multi-molecular associations of H84T-BanLec dimers with the SARS-CoV-2 spike trimer. Single-molecule force spectroscopy demonstrates binding of H84T-BanLec to multiple SARS-CoV-2 spike mannose sites with high affinity, and that H84T-BanLec competes with SARS-CoV-2 spike for binding to cellular ACE2. Modelling experiments identify distinct high-mannose glycans in spike recognized by H84T-BanLec. The multiple H84T-BanLec binding sites on spike likely account for the activity against SARS-CoV-2 variants and the lack of resistant mutants. The broad-spectrum H84T-BanLec should be clinically evaluated in respiratory viral infections including COVID-19.

Coronaviruses exploit a host cysteine-aspartic protease for efficient replication (preprint)

Highly pathogenic coronaviruses including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)1,2, Middle East respiratory syndrome coronavirus (MERS-CoV)3,4, and SARS-CoV-15 vary in their transmissibility and pathogenicity. However, infection by all three viruses result in substantial apoptosis in cell culture6-8 and in patient samples9-11, suggesting a potential link between apoptosis and the pathogenesis of coronaviruses. To date, the underlying mechanism of how apoptosis modulates coronavirus pathogenesis is unknown. Here we show that a cysteine-aspartic protease of the apoptosis cascade, caspase-6, serves as an essential host factor for efficient coronavirus replication. We demonstrate that caspase-6 cleaves coronavirus nucleocapsid (N) proteins, generating N fragments that serve as interferon (IFN) antagonists, thus facilitating virus replication. Inhibition of caspase-6 substantially attenuates the lung pathology and body weight loss of SARS-CoV-2-infected golden Syrian hamsters and improves the survival of mouse-adapted MERS-CoV (MERS-CoVMA)-infected human DPP4 knock-in (hDPP4 KI) mice. Overall, our study reveals how coronaviruses exploit a component of the host apoptosis cascade to facilitate their replication. These results further suggest caspase-6 as a potential target of intervention for the treatment of highly pathogenic coronavirus infections including COVID-19 and MERS.