Anti-Papillomavirus Monoclonal antibody, Clone D2Q6

Background SARS-coronavirus-2 enters host cells through binding of the Spike protein to ACE2 receptor and subsequent S priming by the TMPRSS2 protease. We aim to assess differences in both ACE2 and TMPRSS2 expression in normal tissues from oral cavity, pharynx, larynx and lung tissues as well as neoplastic tissues from the same areas. Methods The study has been conducted using the TCGA and the Regina Elena Institute databases and validated by experimental model in HNSCC cells. We also included data from one COVID19 patient who went under surgery for HNSCC. Results TMPRSS2 expression in HNSCC was significantly reduced compared to the normal tissues. It was more evident in women than in men, in TP53 mutated versus wild TP53 tumors, in HPV negative patients compared to HPV positive counterparts. Functionally, we modeled the multivariate effect of TP53, HPV, and other inherent variables on TMPRSS2. All variables had a statistically significant independent effect on TMPRSS2. In particular, in tumor tissues, HPV negative, TP53 mutated status and elevated TP53-dependent Myc-target genes were associated with low TMPRSS2 expression. The further analysis of both TCGA and our institutional HNSCC datasets identified a signature anti-correlated to TMPRSS2. As proof-of-principle we also validated the anti-correlation between microRNAs and TMPRSS2 expression in a SARS-CoV-2 positive HNSCC patient tissues Finally, we did not find TMPRSS2 promoter methylation. Conclusions Collectively, these findings suggest that tumoral tissues, herein exemplified by HNSCC and lung cancers might be more resistant to SARS-CoV-2 infection due to reduced expression of TMPRSS2. These observations may help to better assess the frailty of SARS-CoV-2 positive cancer patients.

Head and neck squamous cell carcinoma (HNSCC) is malignancy which impairs the life quality of patients and seriously threatens human life. HPV infection has increasingly been recognized as a significant etiology for HNSCC initiation and progression. Emerging evidences have suggested that HPV + and HPV- HNSCC patients showed different responses to cancer therapy, which may be attributed to varied immune cell infiltration in tumor microenvironment. In the present study, we made a comprehensive analysis of significant genes and immune cell infiltration in HNSCC with different HPV status. Firstly, transcriptome data of HNSCC samples with available HPV status was downloaded from The Gene Expression Omnibus (GEO) database and differential expression analysis was performed. A total of 61 differentially expressed genes (DEGs) including 32 upregulated and 29 downregulated genes were identified in HPV + HNSCC when compared to HPV- HNSCC. Further enrichment analysis demonstrated these DEGs were closely associated with cancer-related biological functions and signaling pathways. Infiltration of 22 kinds of immune cells was evaluated by CIBERSORT based on gene expression matrix. As a result, it was indicated that the infiltration of follicular helper T cells, gamma delta T cells, monocytes, eosinophils and neutrophils presented significantly differences between HPV + and HPV- HNSCC. Collectively, our findings may provide new evidences for the development of immunotherapy and personalized precision medicine for HNSCC with different HPV status.