Patients with cancer receiving systemic anti-cancer treatments have been generally assumed by many to be at a higher risk from the disease than their counterparts are who are not receiving anticancer treatment. However, their risk of morbidity and mortality from COVID-19 as a consequence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is not uniform across the world. The evidence to support this claim is scarce and limited to retrospective series arising from China, the epicenter of the COVID-19 pandemic, and involving small numbers of patients. However, despite these severe limitations, the promulgation of this hypothesis has led to widespread global changes to patterns of prescribing chemotherapy and anticancer treatment. In a global health emergency, oncologists, must secure evidence from a large datasets, which can then inform their risk-benefit analyses for individual patients in terms of the use of anticancer treatments. On March 18, 2020, the investigators launched the UK Coronavirus Cancer Monitoring Project (UKCCMP), with widespread support across our national cancer network. 8 Within 5 weeks, the UKCCMP had generated the largest prospective database of COVID-19 in patients with cancer that had been generated to date. the investigators aimed to describe the clinical and demographic characteristics and COVID-19 outcomes in this cohort of patients with cancer and symptomatic COVID-19, and attempted to assess how the presence of cancer and the receipt of cytotoxic chemotherapy and other anticancer treatments affects the COVID-19 disease phenotype.

New Taipei City Municipal TuCheng Hospital has established a special infectious pneumonia ward in May 2021 to treat patients infected with symptomatic SARS-CoV-2 patients. During the period, 97 patients were admitted and treated with 10 infection-related deaths. In light of the current timing of the pandemic, most published serological studies are predominantly cross-sectional, or at most, include a longitudinal follow-up of few months. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has spread globally over the past year, infecting an immunologically naive population and causing significant morbidity and mortality. Immunity to SARS-CoV-2 induced either through natural infection or vaccination has been shown to afford a degree of protection against reinfection and/or reduce the risk of clinically significant outcomes. Seropositive recovered subjects have been estimated to have 89% protection from reinfection, and vaccine efficacies from 50 to 95% have been reported. However, the duration of protective immunity is presently unclear, primary immune responses are inevitably waning, and there is ongoing transmission of increasingly concerning viral variants that may escape control by both vaccine-induced and convalescent immune responses.

Age is considered one of the most crucial covariates that affect phenotypes. However, aging rate may vary among different populations due to genetic variation or miscellaneous environmental exposures. Chronological age is not a perfect proxy for the true biological aging status of the body. A new biological aging measure, phenotypic age (PhenoAge), has been shown to capture morbidity and mortality risk in the general US population and diverse subpopulations. However, how the phenotypic age affect host immunity is not well investigated.

There are currently no effective therapies for SARS-CoV-2, which causes severe respiratory illness or death. Serum neutralizing antibodies rapidly appear after SARS-CoV-2 infection and vaccination. However, little was known about the change of protective antibody titers both to nature infection and post vaccination. And there is ongoing transmission of increasingly concerning viral variants that may escape control by both vaccine-induced and convalescent immune responses. Defining the antibody response to SARS-CoV-2 in patients with cancer receiving anti-cancer therapy, (including chemotherapy, targeted therapy and immunotherapy) will be essential for understanding infection progression, long-term immunity, vaccine efficacy and how phenotypic age affect associated antibodies.