Cancer as a prospective sequela of long COVID‐19

Abstract

As the spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) continues to surge worldwide, our knowledge of coronavirus disease 2019 (COVID-19) is rapidly expanding. Although most COVID-19 patients recover within weeks of symptom onset, some experience lingering symptoms that last for months ("long COVID-19"). Early reports of COVID-19 sequelae, including cardiovascular, pulmonary, and neurological conditions, have raised concerns about the long-term effects of COVID-19, especially in hard-hit communities. It is becoming increasingly evident that cancer patients are more susceptible to SARS-CoV-2 infection and are at a higher risk of severe COVID-19 than the general population. Nevertheless, whether long COVID-19 increases the risk of cancer in those with no prior malignancies, remains unclear.Given, the disproportionate impact of the disease on the African American community, yet another unanswered question is whether racial disparities are to be expected in COVID-19 sequelae. Herein, we propose that long COVID-19 may predispose recovered patients to cancer development and accelerate cancer progression. This hypothesis is based on growing evidence of the ability of SARS-CoV-2 to modulate oncogenic pathways, promote chronic low-grade inflammation, and cause tissue damage. Comprehensive studies are urgently required to elucidate the effects of long COVID-19 on cancer susceptibility.

Blood Cytokine Analysis Suggests That SARS-CoV-2 Infection Results in a Sustained Tumour Promoting Environment in Cancer Patients

“…A recent study has also showed sustained immune dysregulation in haematological cancer patients displaying heterogeneous humoral responses and an exhausted T cell phenotype up to three months after in SARS-CoV-2 exposure [15]. Together these data provide evidence for the need for increased vigilance in clinical follow up for any sequelae of faster cancer progression after SARS-CoV-2 infection in patients with haematological malignancies, as has been speculated recently [48][49][50].…”

Can SARS-CoV-2 induce hematologic malignancies in predisposed individuals? A case series and review of the literature

“…In addition to the influence of SARS‐CoV‐2 on the RAS, other mechanisms could underlie its potential to hasten cancer development. 33 , 34 In a 2012 study, Bhardwaj et al demonstrated that the coronavirus nonstructural protein 15 (Nsp15) can interact with the retinoblastoma protein (pRb), a well-known tumor suppressor, leading to decreased overall levels of pRb. 35 In a 2016 study, Ma-Lauer et al reported that the coronavirus nonstructural protein 3 (Nsp3) stabilizes E3 ubiquitin ligase ring-finger and CHY zinc-finger domain-containing 1 (RCHY1), augmenting the RCHY1-mediated degradation of p53.…”

“… 36 Additionally, COVID‐19 has been associated with T‐cell depletion and activation of several other tumorigenic pathways, including JAK‐STAT, MAPK and NF‐κB. 33 …”

Cell fusion as a link between the SARS-CoV-2 spike protein, COVID-19 complications, and vaccine side effects

“…However, whether any neoplastic hybrids found in humans [58] are made by viral fusogens, as has been suggested [72][73][74], is yet to be determined. Nonetheless, out of an abundance of caution, it may be reasonable to monitor the incidence and progression of neoplastic lesions in COVID-19 patients closely, as has been proposed [75].…”