Of significant interest was the downregulation of MAL (MYD88 adaptor-like), an integral component of Toll-like receptor (TLR) signalling during pathogen invasion,7 and TRIM16, which regulates inflammasome activity through NLRP1-dependent production of IL-1B (Interleukin) and IL-18.8 ECM1, HSPB8, TGM3, TMPRSS11B, ITGA2, SLC20A2, ANXA11, S100A10 and IGFP3 were significantly downregulated in mortality patients, highlighting the possibility of a suboptimal innate immune response. Enrichment of pathways associated with antiviral inflammatory immune signalling (Figure 2D) and protein–protein interaction analysis highlighting the cellular stress response (Figure 2E,F) highlights the state of active defence in moderate patients and a suboptimal immune response in mortality. A possible counteractive effect is observed by the upregulation of HSPA1A, where HSPA1A leads to inhibition of-Nuclear factor kappa B (NF-κB)-regulated NLR family pyrin domain containing 3 (NLRP3) inflammasome activation, thereby preventing exacerbation of inflammation.10 The mechanism for the deregulated host response due to downregulation of MAL and TRIM16 in mortality patients is also depicted in Figure 4A.