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Article

Investigation of the P1104A/TYK2 Genetic Variant in a COVID-19 Patient Cohort from Southern Brazil

by
Giulianna Sonnenstrahl
1,2,
Eduarda Sgarioni
1,2,
Mayara Jorgens Prado
2,
Marilea Furtado Feira
1,2,
Renan Cesar Sbruzzi
1,2,
Bibiana S. O. Fam
1,2,
Alessandra Helena Da Silva Hellwig
2,3,
Nathan Araujo Cadore
1,2,
Osvaldo Artigalás
4,
Alexandre da Costa Pereira
5,
Lygia V. Pereira
6,7,
Tábita Hünemeier
7,8 and
Fernanda Sales Luiz Vianna
1,2,3,9,*
1
Graduate Program in Genetics and Molecular Biology, Genetics Department, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre 91501-970, RS, Brazil
2
Laboratory of Genomic Medicine, Center of Experimental Research, Hospital de Clínicas de Porto Alegre (HCPA), Porto Alegre 90035-903, RS, Brazil
3
Graduate Program in Medical Sciences, Medical Department, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre 91501-970, RS, Brazil
4
Medical Genetics Service, Hospital de Clínicas de Porto Alegre, Porto Alegre 90035-903, RS, Brazil
5
Heart Institute, Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo 05403-000, SP, Brazil
6
Department of Genetics and Evolutionary Biology, Institute of Biosciences, Universidade de São Paulo, São Paulo 05508-090, SP, Brazil
7
National Laboratory of Embryonic Stem Cells, Universidade de São Paulo, São Paulo 05508-090, SP, Brazil
8
Laboratory of Human Population Genomics, Universidade de São Paulo, São Paulo 05508-090, SP, Brazil
9
INAGEMP, National Institute of Populational Medical Genetics, Porto Alegre 90035-903, RS, Brazil
*
Author to whom correspondence should be addressed.
COVID 2025, 5(8), 126; https://doi.org/10.3390/covid5080126
Submission received: 1 July 2025 / Revised: 27 July 2025 / Accepted: 1 August 2025 / Published: 5 August 2025
(This article belongs to the Section Host Genetics and Susceptibility/Resistance)
Review Reports Versions Notes

Abstract

The P1104A variant in the TYK2 gene is recognized as the first common monogenic cause of tuberculosis, and recent studies also suggest a potential role in COVID-19 severity. However, its frequency and impact in admixed Latin American populations remain underexplored. Therefore, we investigated the P1104A/TYK2 variant in a cohort comprising 1826 RT-PCR-confirmed COVID-19 patients from Southern Brazil. Cases were stratified by severity into non-severe (n = 1190) and severe (n = 636). Three homozygous individuals were identified—one non-severe and two severe cases—although no statistically significant association with disease severity was observed. The frequency of the C allele in the COVID-19 cohort (2.85%) was significantly higher than in Brazilian population databases, including “DNA do Brasil” (1.81%, p < 0.001) and ABraOM (2.34%, p = 0.03), but lower than in the multi-ancestry gnomAD database (3.71%, p = 0.01), possibly reflecting ancestry bias. We also observed associations between COVID-19 severity and sex (p = 0.003), age (p < 0.001), obesity (p < 0.001), diabetes (p < 0.001), and hypertension (p < 0.001). Future studies in larger and more diverse cohorts are needed to characterize the prevalence of the variant in admixed populations and assess its contribution to COVID-19 susceptibility.

1. Introduction

Variability in susceptibility and severity of infectious diseases among individuals is influenced by host genetic factors, particularly rare germline mutations that impair essential immune pathways [1]. These pathogenic genetic variants underpin a subset of conditions termed Inborn Errors of Immunity (IEI), formerly known as primary immunodeficiencies, currently encompassing over 550 monogenic disorders that predispose individuals to severe infections, autoimmunity, and autoinflammation, among other phenotypes [2]. Among these, the TYK2 (Tyrosine Kinase 2) gene, a member of the Janus kinase (JAK) family, plays a critical role in IL-12, IL-23, IFN-α/β (IFN-I), and IL-10 signaling pathways via the JAK-STAT pathway [3,4]. Autosomal recessive (AR) deficiencies in TYK2, caused by loss-of-function (LoF) variants, have been associated with susceptibility to infectious diseases, with phenotypic outcomes depending on the affected pathway. Variants impairing IL-12 and IL-23 signaling compromise IFN-γ-mediated immunity, increasing susceptibility to mycobacterial infections such as tuberculosis (TB) and Mendelian Susceptibility to Mycobacterial Disease (MSMD) [5,6]. Defects in IFN-I pathways increase vulnerability to viral infections [7], while IL-10 signaling dysregulation appears clinically silent [8,9].
The P1104A missense variant in the TYK2 gene (P1104A/TYK2, rs34536443), located in the kinase domain of the protein, is a functional polymorphism that reduces TYK2 signaling, particularly by selectively disrupting IL-23 signaling in the homozygous state [10]. This disruption leads to impaired IL-23-induced IFN-γ production, which is the only shared immunological defect between P1104A homozygotes and individuals with complete TYK2 deficiency [11]. Consequently, the P1104A/TYK2 variant is considered the first common genetic variant that, in homozygosity, acts as a mendelian susceptibility factor to TB, with an estimated penetrance above 50% in endemic areas [10,12]. Interestingly, recent genome-wide association studies (GWAS) have linked P1104A to severe COVID-19, showing that carriers of the risk allele (C) have an increased susceptibility to critical outcomes [13,14,15]. This is likely due to impaired IFN-I-mediated innate immune responses, which are crucial for SARS-CoV-2 control [16]. Supporting this, Dendrou et al. (2016) reported that this variant leads to a near-complete loss of TYK2 function in homozygosity, impairing not only IL-23, but also IL-12 and IFN-I signaling [17]. Importantly, P1104A has also been associated with protection against several autoimmune diseases due to reduced pro-inflammatory signaling [17].
COVID-19, caused by SARS-CoV-2, has emerged as one of the most impacting pandemics of the 21st century, with clinical outcomes ranging from asymptomatic to fatal disease [18,19]. Host genetic factors are known to play a major role in modulating this clinical variability [1,16,20]. However, few studies have investigated the prevalence and impact of P1104A/TYK2 in admixed populations such as the Brazilian population, which exhibits unique genetic diversity resulting from historical admixture among European, African, and Native American ancestries [21]. Therefore, the aim of this study was to investigate the frequency of the P1104A/TYK2 variant in a Brazilian COVID-19 cohort and assess its potential contribution to disease severity in this genetically diverse population.

2. Materials and Methods

2.1. Sample

This study included a total of 1826 patients with RT-PCR-confirmed COVID-19, tested at the Hospital de Clínicas de Porto Alegre (HCPA) between 2020 and 2022. The sample comprises 1376 DNA samples obtained from the HCPA Biobank (https://doi.org/10.22491/hcpa-biobanco-amostras, accessed on 31 July 2025) and 450 whole-genome sequencing samples from individuals enrolled in the “DNA do Brasil” project, approved under CAAEs: 36974620.3.0000.5327 and 30688220.7.0000.5464. A diagnosis of HIV was considered an exclusion criterion. All participants provided written informed consent after being informed about the objectives of the research. The study was approved by the Research Ethics Committee of Hospital de Clínicas de Porto Alegre (project number 2024-0216; CAAE: 81761224.8.0000.5327).

2.2. Clinical and Demographic Data Analysis

Clinical and demographic data were obtained through health record review and included sex, age, self-reported skin color, and presence of comorbidities. Information on comorbidities was retrieved through a structured query that extracted all ICD codes ever recorded in each patient’s electronic health record. Additionally, for a subset of 450 individuals enrolled in the “DNA do Brasil” project, comorbidity information was collected mainly through manual review of health records, with a small portion also completing a questionnaire administered at the time of informed consent. Patients were classified into two groups according to disease severity. The severe group included individuals who developed acute respiratory distress syndrome (ARDS) or required intensive care unit (ICU) admission with mechanical ventilation, and/or evolved to death. The non-severe group included all other patients who did not meet these criteria.

2.3. Genetic Analysis

Genetic analysis was performed using two types of data. For patients from the HCPA Biobank, genotyping of the P1104A/TYK2 variant (rs34536443 [G > C]) was performed using the TaqMan® Genotyping Assay (assay ID: C__60866522_10) on a QuantStudio™ 3 Real-Time PCR system (Applied Biosystems, USA), following the manufacturer’s instructions. For patients from the “DNA do Brasil” project, whole-genome sequencing data were already available and used to determine the genotype at the P1104A/TYK2 locus. Variant calling was based on the hg38 reference genome, and genotypes were extracted from position chr19:10352442.

2.4. Statistical Analysis

Categorical variables were reported as frequencies (percentages) and compared using the Chi-squared test or Fisher’s exact test. Quantitative variables, reported as median (min–max), were tested for normality using the Shapiro–Wilk test, and comparisons between groups were conducted with either Student’s t-test or the Mann–Whitney U test. Hardy–Weinberg equilibrium (HWE) for genetic variants was evaluated using the HWExact function from the HardyWeinberg R package (version 1.7.8). Allelic frequencies were compared between groups within the COVID-19 cohort using the Chi-squared test. Additionally, allelic frequencies were compared with those reported in the Arquivo Brasileiro Online de Mutações (Online Archive of Brazilian Mutations—ABraOM) database (https://abraom.ib.usp.br/, accessed on 31 July 2025), the “DNA do Brasil” project (https://www.dnabr.science/, accessed on 31 July 2025) [21], and the Genome Aggregation Database (gnomAD; https://gnomad.broadinstitute.org/, accessed on 31 July 2025) using the Chi-squared goodness-of-fit test. To avoid data duplication, 485 samples from our COVID-19 cohort that were originally included in the “DNA do Brasil” database were excluded from that database prior to frequency comparisons. Genotypic frequencies were compared between groups using the association function from the SNPassoc R package (version 2.1-2), under the recessive genetic model. Logistic regression models were fitted to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for the association between the P1104A/TYK2 genotype and COVID-19 severity, adjusting for age and sex, known risk factors for severe COVID-19. To assess the statistical power for detecting genetic associations for the P1104A/TYK2 variant and COVID-19 severity, we performed a post hoc power analysis using the genpwr R package (version 1.0.4), based on the observed parameters of our cohort (minor allele frequency = 2.85%; n = 1826; case rate = 34.83%), under a recessive model, assuming an odds ratio of 3.75 and a significance level of 0.05. Additionally, using the same package, we performed a sample size calculation to estimate the number of individuals required to achieve 80% power, under the same parameters. All statistical analyses were conducted in R (version 4.4.2). A p-value < 0.05 was considered statistically significant.

3. Results

The COVID-19 study sample was composed of 1826 individuals classified into non-severe (n = 1190) and severe (n = 636) COVID-19 groups. Clinical and demographic characteristics are summarized in Table 1. Compared to the non-severe group, severe cases were older (p < 0.001) and had a greater proportion of males (p = 0.003). In terms of comorbidities, obesity, diabetes, and hypertension were significantly more prevalent among individuals within the severe group (p < 0.001 for all). As for skin color, chronic heart disease, and chronic kidney disease, no significant differences were observed between groups.
The P1104A/TYK2 variant was in Hardy–Weinberg equilibrium in both groups (Table S1). The frequency of the C allele was slightly lower in severe cases (2.52%) compared to non-severe cases (3.03%), with no statistically significant difference between these groups (p = 0.44), as detailed in Table 2. Interestingly, the allelic frequency of the COVID-19 cohort significantly differed from the population databases evaluated, with the C allele frequency being higher when compared to “DNA do Brasil” and ABraOM databases (p < 0.001 and p = 0.003, respectively), but lower when compared to gnomAD (p = 0.01; Table S1).
We identified three patients harboring the CC genotype for the P1104A/TYK2 variant within our cohort (Table 3). One patient was classified as non-severe, a 63-year-old male with obesity, diabetes mellitus (DM), hypertension, and chronic heart disease, who was hospitalized, required non-invasive ventilation, and survived. The other two patients, both classified as severe, were a 60-year-old male with DM and hypertension who was hospitalized, admitted to the ICU, and developed ARDS, requiring invasive ventilation, and ultimately died, and a 52-year-old male with hyperthyroidism and Graves’ disease who was hospitalized, developed ARDS requiring non-invasive ventilation, and survived. Comparison of genotypic frequencies under the recessive model revealed no significant association with COVID-19 severity, despite a slightly higher frequency of the CC genotype in severe cases (0.31%) compared to non-severe (0.08%). After adjusting for age and sex, the association remained non-significant (Table 4).

4. Discussion

Since the first reports of IEIs in the 1950s, significant progress has been made in understanding the genetic basis of infectious diseases and explaining why some individuals exhibit distinct immune responses to the same pathogen [1,2,22]. This variability is particularly evident in COVID-19, where among unvaccinated individuals, approximately 20% develop moderate to severe symptoms requiring hospitalization, and around 10% progress to critical illness [23,24]. These findings support the role of host genetics in modulating clinical outcomes. In this context, we investigated the P1104A/TYK2 variant in a cohort of Brazilian patients with COVID-19. Three homozygous individuals were identified: one classified as non-severe and two as severe. Although the homozygous genotype was more frequent in the severe group (0.31%) compared to the non-severe group (0.08%), this difference was not statistically significant (p = 0.26). Additionally, it is possible that the immunological effects of P1104A/TYK2 are less relevant in the context of viral infections. While previous studies have shown that this variant may impair IL-12 and IFN-I signaling in some experimental settings [17], the physiological relevance appears limited. Indeed, individuals with complete TYK2 deficiency typically exhibit impaired responses to IL-12, IL-23, and IFN-I, resulting in increased susceptibility to intracellular bacteria and a wide range of viral infections, including herpesviruses [6]. In contrast, homozygous carriers of the P1104A variant exhibit impaired IL-23 responses, while IFN-I signaling appears only partially affected [10,12]. This partial functional impairment may be sufficient to predispose to mycobacterial infections, such as tuberculosis, but insufficient to significantly compromise antiviral immunity, particularly SARS-CoV-2, which relies heavily on early and effective IFN-I responses [16,17]. This might also explain the absence of a strong statistically significant association between P1104A variant and COVID-19 severity.
It is believed that the P1104A/TYK2 variant emerged 30,000 years ago in Europe, preceding the occupation of the Americas, which began approximately 20,000 years ago [12,25]. Subsequently, historical events such as the transatlantic slave trade and intense European migration resulted in significant interactions between populations that had previously been genetically isolated [25]. In Latin America, this resulted in highly admixed populations with diverse genetic backgrounds. In Brazil, the genetic ancestry of the population was predominantly shaped by three parental populations—European (EUR), African (AFR), and Native American (AMR)—with varying proportions across geographic regions [15,21,26]. In this context, we observed a significantly higher frequency of the C allele in the COVID-19 cohort (2.85%) compared to Brazilian population databases (“DNA do Brasil” = 1.81%; ABraOM = 2.34%), which is likely influenced by the ancestry patterns reflected by the geographic origin of the samples. For instance, the “DNA do Brasil” project includes individuals from all regions of Brazil (EUR: 68.10%), while ABraOM is composed of elderly individuals from São Paulo (southeast region—EUR: 69.10%) [21,26]. In contrast, our COVID-19 cohort consists of individuals from the state of Rio Grande do Sul (south region—EUR: 80.00%), where European ancestry is more prevalent, possibly explaining the higher frequency of the C allele in our cohort [26]. It is important to note that, within the “DNA do Brasil” database, one of the sub-cohorts originally representing the state of Rio Grande do Sul comprised 485 COVID-19 samples that overlapped with our dataset. Although only 450 of them met the inclusion criteria and were considered in our study, all 485 were excluded from the “DNA do Brasil” database in order to avoid data duplication. As a result, the only remaining Rio Grande do Sul sub-cohort in the “DNA do Brasil” project consists of self-declared Black individuals with chronic kidney disease, which limits the representativeness of the general population of Rio Grande do Sul in that database. Notably, the frequency of the C allele in the “DNA do Brasil” database was 2.00% when the overlapping samples were included, but decreased to 1.81% after their removal, a difference likely driven by the ancestral background of the COVID-19 cohort samples. When compared to gnomAD, which reports a C allele frequency of 3.71%, our cohort exhibited a significantly lower frequency, which is likely attributed to the overrepresentation of individuals with European ancestry in gnomAD [27]. These findings highlight the importance of considering ancestry in genetic studies, especially in highly admixed populations such as Brazil’s, and reinforce the need for more representative population-specific genomic databases to ensure accurate allele frequency estimates and minimize ancestry-related biases. Interestingly, prior research has demonstrated a marked decline in the frequency of the P1104A/TYK2 variant over the last 4000 years in Europe due to strong negative selection driven by endemic tuberculosis [10,28]. Given that Brazil remains a TB-endemic country [29], it is plausible that this variant may still be under similar evolutionary pressure, potentially influencing its frequency in the population over time.
Severe COVID-19 outcomes have been consistently associated with a combination of host genetics and demographic and clinical factors [30,31]. We observed that individuals with severe disease were older and more frequently male compared to non-severe cases, a pattern that mirrors findings from large-scale studies [32,33,34,35]. While infection rates between sexes are similar, men are at significantly higher risk of developing severe disease and death, likely due to a weaker early response to COVID-19, characterized by lower IFN-I production [36,37], and a less robust adaptive immune system [38,39,40] when compared to females, among other factors. Advanced age is another well-established risk factor for severe COVID-19, largely due to immunosenescence, characterized by reduced IFN-I activity and chronic inflammation (inflammaging), which weakens antiviral defenses [41,42,43]. This vulnerability is further amplified by additional factors, such as pre-existing comorbidities commonly associated with aging and the presence of neutralizing autoantibodies against IFN-I [44]. Furthermore, comorbidities such as obesity, diabetes, and hypertension were markedly more frequent among severe cases and some pathophysiological mechanisms may explain the association between these comorbidities and COVID-19 severity, including increased Angiotensin Converting Enzyme-2 (ACE-2) expression in adipose tissue, potentially acting as a viral reservoir, and the pro-inflammatory state associated with this conditions [45,46,47,48,49,50,51,52]. Interestingly, we did not identify a significant association between COVID-19 severity and chronic kidney disease, chronic heart disease, or chronic pulmonary disease. It is worth mentioning that information on some chronic conditions was limited, with data available for only 31.00% individuals regarding chronic kidney disease, 30.07% for chronic heart disease, and 24.70% for chronic pulmonary disease, which may have impacted the detection of associations with COVID-19 severity [53,54,55].
This study has some limitations that should be considered. First, despite the relatively large total sample size, the number of homozygous individuals and severe cases was small, reducing the statistical power to detect associations. The power analysis revealed that the study had only 12.38% power to detect an odds ratio of 3.75 at a significant level of 0.05 under a recessive model, given the observed parameters. Therefore, the absence of a statistically significant association between P1104A/TYK2 and COVID-19 severity should not be interpreted as conclusive evidence of no effect, but rather as a reflection of limited statistical power. To estimate the sample size required to adequately assess this association, we performed a sample size calculation, which revealed that approximately 23,000 individuals would be required to achieve 80% power, under the same conditions. It is worth noting that a previous study of TB cases and controls [12] reported an ancestry-adjusted odds ratio of 5, based on more than 100,000 controls. Second, the lack of more comprehensive clinical information for a subset of participants limited the characterization of their comorbidities and may have affected the accuracy of severity classification. Additionally, since the retrieval of diagnostic information relied mostly on the availability and quality of routine documentation, and because the absence of information did not necessarily indicate the absence of a given condition, the completeness of data was limited, which may have led to an underestimation of the impact of these conditions in COVID-19 severity. Third, our sample was geographically limited to a single Brazilian state, which may restrict the generalizability of our findings to other regions with different ancestry profiles.

5. Conclusions

This study provides one of the first insights into the frequency and potential impact of the P1104A/TYK2 variant in a highly admixed Brazilian population affected by COVID-19. Our findings emphasize the importance of accounting genetic ancestry in association studies in admixed populations and underscore the need for more representative population databases in Brazil. Further investigations in larger and more diverse cohorts are required to clarify the role of the P1104A/TYK2 variant in COVID-19 susceptibility. Given the geographic and genetic diversity of Brazil, future multi-centric studies across different regions can improve the understanding of host genetic factors in COVID-19 outcomes, and refine risk prediction in Latin American populations. In addition, our findings corroborate that age, sex, and comorbidities such as obesity, diabetes, and hypertension remain key predictors of COVID-19 severity.

Supplementary Materials

The following supporting information can be downloaded at https://www.mdpi.com/article/10.3390/covid5080126/s1, Table S1: Hardy–Weinberg equilibrium and allelic frequency comparison with population databases.

Author Contributions

Conceptualization, F.S.L.V. and O.A.; Methodology, G.S. and E.S.; Formal analysis, E.S. and G.S.; Investigation, G.S., M.F.F., M.J.P., A.H.D.S.H., R.C.S., N.A.C., and B.S.O.F.; Resources, F.S.L.V., A.d.C.P., L.V.P., and T.H.; Data curation, G.S., E.S., and M.J.P.; Writing—original draft preparation, G.S. and F.S.L.V.; Writing—review and editing, F.S.L.V., M.J.P., B.S.O.F., E.S., O.A., and R.C.S.; Supervision, F.S.L.V. All authors have read and agreed to the published version of the manuscript.

Funding

This study received funding from Financiamento e Incentivo à Pesquisa (FIPE/HCPA), Hospital de Clínicas de Porto Alegre (grant number 2024-0216) and from Brazilian National Program of Genomics and Precision Health–Genomas Brasil, Departamento de Ciência e Tecnologia da Secretaria de Ciência, Tecnologia e Inovação e do Complexo Econômico-Industrial da Saúde do Ministério da Saúde (Decit/SECTICS/MS) (888379/2019). F.S.L.V. is the recipient of a Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) scholarship 312960/2021-2, and G.S. is the recipient of CAPES scholarships 88887.802747/2023-00.

Institutional Review Board Statement

The study was approved by the Research Ethics Committee of Hospital de Clínicas de Porto Alegre (project number 2024-0216; CAAE: 81761224.8.0000.5327).

Informed Consent Statement

Informed consent was obtained from all subjects involved in this study.

Data Availability Statement

Part of the data analyzed in this study originates from the “DNA do Brasil” project, which has been previously described and published [21].

Conflicts of Interest

The authors declare no conflicts of interest.

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Table 1. Demographic and clinical characteristics of cases within the COVID-19 cohort.
Table 1. Demographic and clinical characteristics of cases within the COVID-19 cohort.
Non-Severe
n = 1190 (%)		Severe
n = 636 (%)		p-Value
SexMale552 (46.39)342 (53.77)0.003
Female638 (53.61)294 (46.23)
Age 57 (19–100)62 (19–102)<0.001
Skin colorWhite983/1186 (82.89)517/635 (81.42)0.35
Black194/1186 (16.36)109/635 (17.17)
Other9/1186 (0.75)9/635 (1.41)
ComorbiditiesChronic Heart Disease131/376 (34.84)63/173 (36.42)0.79
Chronic Kidney Disease132/384 (34.38)63/182 (34.62)1.00
Chronic Pulmonary Disease52/301 (17.27)27/150 (18.00)0.95
Obesity87/290 (30.00)101/185 (54.59)<0.001
Diabetes68/309 (22.01)87/179 (48.60)<0.001
Hypertension168/370 (45.41)163/222 (73.42)<0.001
Values are presented as n (%) or as median (min–max). Statistical tests used include the Chi-squared test, Chi-squared test with Yates’ correction, and Mann–Whitney U test, as appropriate. Statistically significant p-values are highlighted in bold.
Table 2. Comparison of the P1104A/TYK2 allelic frequencies between groups.
Table 2. Comparison of the P1104A/TYK2 allelic frequencies between groups.
AlleleNon-Severe (%)Severe (%)p-Value
G2308 (96.97)1240 (97.48)0.44
C72 (3.03)32 (2.52)
Values are presented as n (%). Allele frequency comparison was performed using the Chi-squared test.
Table 3. Genotypic frequencies of P1104A/TYK2 under a recessive model between groups.
Table 3. Genotypic frequencies of P1104A/TYK2 under a recessive model between groups.
Non-Severe
n = 1190 (%)		Severe
n = 636 (%)		OR (95% CI)p-ValueAIC
GG–GC1189 (99.92)634 (99.69)1.000.262363
CC1 (0.08)2 (0.31)3.75 (0.34–41.44)
Values are presented as n (%). Columns: OR (odds ratio), CI (95% confidence interval), and AIC (Akaike Information Criterion).
Table 4. Logistic regression adjusted for age and sex.
Table 4. Logistic regression adjusted for age and sex.
OR95% CIp-Value
CC genotype3.340.32–72.030.33
Male sex1.271.05–1.550.01
Age1.021.01–1.02<0.001
Columns: OR (odds ratio), CI (95% confidence interval). Statistically significant p-values are highlighted in bold.
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Sonnenstrahl, G.; Sgarioni, E.; Prado, M.J.; Feira, M.F.; Sbruzzi, R.C.; Fam, B.S.O.; Da Silva Hellwig, A.H.; Cadore, N.A.; Artigalás, O.; da Costa Pereira, A.; et al. Investigation of the P1104A/TYK2 Genetic Variant in a COVID-19 Patient Cohort from Southern Brazil. COVID 2025, 5, 126. https://doi.org/10.3390/covid5080126

AMA Style

Sonnenstrahl G, Sgarioni E, Prado MJ, Feira MF, Sbruzzi RC, Fam BSO, Da Silva Hellwig AH, Cadore NA, Artigalás O, da Costa Pereira A, et al. Investigation of the P1104A/TYK2 Genetic Variant in a COVID-19 Patient Cohort from Southern Brazil. COVID. 2025; 5(8):126. https://doi.org/10.3390/covid5080126

Chicago/Turabian Style

Sonnenstrahl, Giulianna, Eduarda Sgarioni, Mayara Jorgens Prado, Marilea Furtado Feira, Renan Cesar Sbruzzi, Bibiana S. O. Fam, Alessandra Helena Da Silva Hellwig, Nathan Araujo Cadore, Osvaldo Artigalás, Alexandre da Costa Pereira, and et al. 2025. "Investigation of the P1104A/TYK2 Genetic Variant in a COVID-19 Patient Cohort from Southern Brazil" COVID 5, no. 8: 126. https://doi.org/10.3390/covid5080126

APA Style

Sonnenstrahl, G., Sgarioni, E., Prado, M. J., Feira, M. F., Sbruzzi, R. C., Fam, B. S. O., Da Silva Hellwig, A. H., Cadore, N. A., Artigalás, O., da Costa Pereira, A., Pereira, L. V., Hünemeier, T., & Vianna, F. S. L. (2025). Investigation of the P1104A/TYK2 Genetic Variant in a COVID-19 Patient Cohort from Southern Brazil. COVID, 5(8), 126. https://doi.org/10.3390/covid5080126

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