Data within the graphs represent correlations between D-dimer and the (A) anti-NP or (B) anti-RBD IgG Fab. and RBD were associated with disease severity among the individuals with this study. MAIN CONCLUSIONS Our data suggest that IgG against NP and RBD participates in the worsening of COVID-19. Even though humoral response against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is usually partially comprehended, and more efforts are needed to clarify gaps in the knowledge of this process. Key words: D-dimer, coagulopathy, immunoglobulin humoral response, SARS-CoV-2, COVID-19 The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is an enveloped computer virus with single-stranded RNA that is the etiological agent of coronavirus disease 2019 (COVID-19). SARS-CoV has four structural proteins, namely the spike (S), envelope (E), membrane (M) and nucleocapsid phosphoprotein (NP). 1 The S protein is necessary for viral access into host cells as it contains the receptor-binding domain name (RBD). 2 The RBD is usually part of the S1 subunit of the S protein and comprises the fragment that binds to the human angiotensin-converting enzyme 2 (ACE2) present around the cell surface. 2 ACE2 plays a central role as the cellular receptor for viral access into the cell. NP recovers the viral genomic RNA and impairs host effector mechanisms of viral RNA degradation. 3 , 4 As viral access into the human cell depends on the conversation between the RBD and ACE2, antibodies specifically targeting this domain name have high neutralising activity against the computer virus. In contrast, antibodies against NP, cannot neutralise the computer virus. WP1130 (Degrasyn) 5 Previous studies on SARS-CoV found an association between high titres of anti-NP antibodies and poor outcomes in infected patients. 6 , 7 However, no mechanism has been suggested to explain the relationship between severity and the humoral response against NP. In this context, antibodies against the RBD protein of SARS-CoV may protect the organism against contamination, while antibodies targeted at other regions of the S protein may even enhance contamination. 8 A mechanism that may be associated with the pathophysiology of the disease is the onset of systemic coagulation, which involves the emergence of thrombotic events, such as deep vein thrombosis (DVT) and pulmonary WP1130 (Degrasyn) embolism (PE), alongside arterial and systemic thrombosis or even during extracorporeal membrane oxygenation (ECMO) treatment in extracorporeal circuits. In this regard, it was shown that such patients have antibodies that can trigger a coagulation cascade like a haemophagocytic syndrome. 9 , 10 Herein, we investigated the titres of immunoglobulins in patients with different clinical forms of COVID-19 as indicated by circulating D-dimer levels in the patient plasma. We also describe the production of specific IgGs against the nucleoprotein (NP) and the receptor binding domain name (RBD) of the spike protein of SARS-CoV-2 in patients with different clinical forms of COVID-19. MATERIALS AND BMP2 METHODS – The Research Ethics Committee of UFOB approved this study in 2020 (license number: 30629520.6.0000.0008). All clinical investigations were conducted according to the Declaration of Helsinki. – This was a cross-sectional study of COVID-19 cases registered in cities in the western region of Bahia, Brazil, from May to October 2020. Available laboratory and clinical data from non-infected health professionals (n = 9) and patients with oligosymptomatic (n = 22) and severe (n = 30) disease at the Hospital do Oeste were collected. The exclusion criterion for infected WP1130 (Degrasyn) patients was the absence of a confirmation of the disease by quantitative polymerase chain reaction (qPCR). Clinical data were collected from patients in the cured group (n = 27) through interviews; additionally, blood samples were collected from patients. Then, an immune enzymatic assay was performed to detect different isoforms of immunoglobulins as explained below. – Swab samples obtained from patients reporting COVID-19-like symptoms were processed for SARS-CoV-2 detection via quantitative real-time PCR (RT-qPCR) using the USCDC protocol. In brief, sample RNA was extracted using commercial.