Human T-cell lymphotropic virus type-I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP), the main neurological manifestation of HTLV-I, is a chronic inflammatory disease. Viral-host interaction and host genetics are two important contributors to the development of the HAM/TSP. This study was conducted to measure the serum level of tumor necrosis factor-alpha-like weak inducer of apoptosis (TWEAK) by ELISA method in three groups of participants including 34 HAM/TSP patients (HAM/TSP), 35 asymptomatic HTLV-1 carriers (ACs), and 20 healthy controls (HCs). Also, the titer of the proviral load in two groups of HAM/TSP and ACs was assessed by the real-time polymerase chain reaction (PCR). The statistical results showed that, there is no significant difference between the three groups in TWEAK cytokine level ( = 0.667). Also, there was no significant difference in proviral load titer between groups of HAM/TSP and ACs ( = 0.08). Furthermore, no significant difference was observed between proviral load and TWEAK cytokine concentration between groups of HAM/TSP and ACs. Our findings showed that despite the inflammatory nature of HAM/TSP disease, the expression level of TWEAK in HAM/TSP patients is not significantly different from the groups of ACs and HCs. Therefore, the involvement of other factors in causing HAM/TSP is not unexpected.

This study investigates the demographic, clinical characteristics, virological profiles, and immunological responses of patients with viral encephalitis (VE) compared with a control group. The VE group displayed a wide range of neurological symptoms. Virological analysis revealed the predominance of Herpesviridae family viruses. Immune responses in cerebrospinal fluid (CSF) from patients with VE were examined, highlighting an immunological shift toward T helper 1 (Th1) cells dominance, altered T helper 17 cells/regulatory T cells (Th17/Tregs) balance, and high interleukin-6 expression. These findings provide insights into the complex immunological landscape of VE, highlighting the role of specific cytokines and T cell subsets in its pathogenesis and potentially guiding targeted therapeutic strategies.

This study aims to evaluate the estimate of causal relationship between Epstein-Barr virus (EBV) antibody levels and autoimmune diseases (AIDs), such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), through bidirectional two-sample Mendelian randomization (MR) analysis. Despite 50 years of research into the link between EBV infection and AIDs, inconsistent results persist due to the complex mechanisms of EBV within the body. We utilized large-scale genome-wide association studies (GWAS) data from the Integrative Epidemiology Unit (IEU) Open GWAS Project database to conduct rigorous MR analysis, incorporating various sensitivity analyses to assess potential impacts and ensure robustness. EBV antibodies (including VCA-IgG, ZEBRA-IgG, EBNA-1-IgG, and EA-D-IgG) were used as exposure variables, whereas RA and SLE served as outcome variables. In the reverse analysis, RA and SLE were treated as exposure variables and EBV antibodies as outcome variables. When EBV antibodies are designated as the exposure variables, the random-effects inverse-variance weighted (IVW) analysis indicated a significant negative genetic causal relationship between EBV EA-D antibody levels and RA ( = 0.007, odds ratio [OR] = 0.700, 95% confidence interval [CI] = [0.539-0.907]). No significant genetic causal relationship was found between SLE and EBV antibody levels. When RA and SLE are designated as the exposure variables, the random-effects IVW analysis revealed significant positive genetic causal relationships between SLE and EBV ZEBRA antibody levels ( = 0.009, OR = 1.028, 95% CI = [1.007-1.050]) and EBV EA-D antibody levels ( = 0.005, OR = 1.032, 95% CI = [1.009-1.054]). No significant genetic causal relationship was observed between RA and EBV antibody levels. This study offers compelling evidence of a causal relationship between EBV antibody levels and AIDs through MR analysis. Our findings lay a new foundation and perspective for future research directions, clinical prognosis, and treatment.

The SARS-CoV-2 pandemic has confirmed that the ability to rapidly mutate may be extremely beneficial for a virus. Not long after the first wave, new variants emerged with altered infectivity, disease severity, and mortality. These new strains most notably had numerous mutations of the spike (S) protein, a surface protein responsible for binding to and entering the host cell. The Delta and Omicron strains demonstrated increased immune evasion and improved binding affinity to the host cell receptor, angiotensin-converting enzyme 2 (ACE2). This study examines the ability of wild-type SARS-CoV-2 IgG to bind Delta and Omicron antigens, as well as their functional binding capabilities to two different S-ACE2 complexes. Twenty SARS-CoV-2 positive samples from patients who had recovered from infection with ancestral SARS-CoV-2 in the first wave of COVID-19 and 10 pre-pandemic control samples were studied. SARS-CoV-2 exposed patients showed significantly higher levels of IgG to SARS-CoV-2 S1/RBD ( < 0.001), N protein ( < 0.001), and Omicron spike variant ( = 0.01), but not to Delta spike variant ( = 0.966) when compared with controls. Furthermore, patient samples showed significantly greater inhibition of SARS-CoV-2 S1/RBD and E484K spike to ACE2 binding ( < 0.001 and = 0.015, respectively). Conversely, there was no correlation between the binding inhibition of S1/RBD and E484K spike to ACE2 receptor. This study shows there is considerable cross-reactivity of IgG generated by wild-type SARS-CoV-2 infection to the Delta and Omicron variants.

The plausible effects of SARS-CoV-2 infection on the expression of anti/proapoptotic molecules have been suspected. This cohort study examined the expression of p53, Bcl-2, Bid, Bak, and Bax molecules, the genes associated with induction or inhibition of apoptosis, in the SARS-CoV-2-infected patients with severe and mild symptoms in an Iranian population. In this 6-month cohort study, the expression of p53, Bcl-2, Bid, Bak, and Bax molecules was evaluated at onset of diagnosis, 24 h after symptom onset, and 6 months later in the nasopharyngeal cells of SARS-CoV-2-infected hospitalized patients and outpatients in comparison with healthy controls using the real-time PCR technique. At the onset of the study, the relative expression of p53, Bcl-2, Bid, Bak, and Bax significantly increased in the SARS-CoV-2-infected hospitalized patients and decreased after 6 months. The healthy controls showed potential positive correlations among the molecules, but the patients did not show these correlations. Since SARS-CoV-2 needs host cell survival, it appears that the virus induces the expression of Bcl-2 as an antiapoptotic molecule, and the host cells upregulate the proapoptotic molecules to neutralize the effects. Dysregulation of correlation expression of the molecules among the patients proved that SARS-CoV-2 affects the expression of the molecules involved in apoptosis. SARS-CoV-2 could be considered an important factor that regulates the expression of several molecules participating in cancer pathogenesis.

The COVID-19 pandemic has affected the global health system and economies largely. Therefore, knowledge about the clinical and laboratory profiles of patients with COVID-19 would help in the management and prognosis of the disease. The immunological and hematological indices have emerged as critical determinants for the severity of the disease and the prognosis; however, association with COVID-19 is clouded. The present study is aimed to characterize the immunological and hematological profiles of patients with COVID-19 in correlation with the disease severity. The study included 1,019 polymerase chain reaction (PCR)-confirmed patients with COVID-19 who were classified into serious and nonserious groups, considering severity criteria. Clinical laboratory investigations included hematological, biochemical, and immunological parameters regarding leukocyte counts, hemoglobin levels, and inflammatory markers. Our analysis of immunological and hematological differences between serious and nonserious patients with COVID-19 indicates that serious cases reflected elevated levels of pro-inflammatory markers such as lactate dehydrogenase, C-reactive protein (CRP), D-dimer, and ferritin, representing immune system dysregulation and systemic inflammation. Furthermore, in serious cases, discrepancies had also been noticed for many hematological parameters than nonserious ones, which also contained leukocyte count and hemoglobin level. Additionally, the CRP, D-dimer, blood urea nitrogen, alanine transaminase, and albumin levels could be independent predictors of COVID-19 severity by multivariate logistic regression analysis. Cutoff values for these biomarkers were defined by receiver operating characteristic curve analysis defining optimal parameters for the risk stratification and prognostication. The current investigation provides a comprehensive understanding of immunological and hematological correlation with COVID-19 severity, refining clinical decision-making and therapeutic interventions to improve patient outcomes.

Vaccines have always been a critical tool in preventing infectious diseases. However, the development of traditional vaccines often takes a long time and may struggle to address the challenge of rapidly mutating viruses. The emergence of mRNA technology has brought revolutionary changes to vaccine development, particularly in rapidly responding to the threat of emerging viruses. The global promotion of mRNA vaccines against severe acute respiratory syndrome coronavirus 2 has demonstrated the importance of mRNA technology. Also, mRNA vaccines targeting viruses such as influenza, respiratory syncytial virus, and Ebola are under development. These vaccines have shown promising preventive effects and safety profiles in clinical trials, although the duration of immune protection is still under evaluation. However, the development of mRNA vaccines also faces many challenges, such as stability, efficacy, and individual differences in immune response. Researchers adopt various strategies to address these challenges. Anyway, mRNA vaccines have shown enormous potential in combating viral diseases. With further development and technological maturity, mRNA vaccines are expected to have a profound impact on public health and vaccine equity. This review discussed the potential of mRNA vaccines to fight against viruses, current progress in clinical trials, challenges faced, and future prospects, providing a comprehensive scientific basis and reference for future research.

Viral infections are one of the principal causes of global primary health crises, with increased rate of infection and mortality demonstrated by the newer progeny of viruses. Viral invasion of the host involves utilization of various cellular machinery. Ubiquitination is one of a few central regulatory systems used by viruses for establishment of the infections in the host. Members of the ubiquitination system are involved in carrying out proteasomal degradation or functional modification of proteins in numerous cellular processes. E3 ubiquitin ligases play a major role in this system through recognition and recruitment of protein substrates and catalyzing the transfer of ubiquitin to these substrates. The versatility of ubiquitin ligases frequently makes them useful tools for the viruses, for either utilizing or degrading other cellular machineries, for carrying out their multiplication or inactivating the defensive strategies of the host. Therefore, these ligases are important targets for aiming at major pathways causing viral protein degradation or functional modification of the infection process. In this review, we have discussed the role and mechanism of different types of ubiquitin ligases in the context of infections of mainly human viruses, highlighting the viral proteins directly interacting with the ligases. Knowledge about these direct interactions is central in understanding the ubiquitin-dependent processes. This comprehensive account may also be beneficial for pharmaceutical exploration of E3 ligase-based broad-spectrum antiviral treatment.

Following viral infection, antigen-restricted T lymphocytes are activated and recognize infected cells to eliminate them. A subset of T cells differentiates into memory lymphocytes able to counteract viral rechallenge in a faster and enhanced way. SARS-CoV-2 can escape immune responses leading to a poor clinical outcome. Immune escape can be associated with the failure of the development of T cell memory compartments. The aim of this study is to characterize the T memory subsets and to test the immune response against class I- and II-restricted immunodominant epitopes shared by ancestral and SARS-CoV-2 variants strains. T memory subsets and recognition of SARS-CoV-2S Spike-specific epitopes were analyzed by flow cytometry on 14 fully vaccinated healthy donors (HDV) and 18 COVID-19 recovered patients (CD). The results obtained showed that CD8+ T naïve subset numbers decreased in association with a significant increase of the effector memory T cell subset whereas there was a small increase in the percentage of SARS-CoV-2 antigen-restricted T clones in both CD4 and CD8+ subset in the CD compared to HDV sample. Collectively, these features may reflect a broader cytotoxic T cell repertoire stimulated by the virus during the natural infection compared to the spike-restricted response activated during vaccination.

The enduring impact of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and its disease manifestation, COVID-19, on public health remains significant. Postacute sequelae of SARS-CoV-2 infection (PASC) affect a considerable number of patients, impairing their quality of life. While the role of the cytokine storm in acute COVID-19 is well established, its contribution to the pathophysiology of PASC is not fully understood. This study aimed to analyze the cytokine profile of patients with PASC following stimulation of Toll-like receptor (TLR) pathways, comparing them with a healthy control group. From October 2020 till March 2021, Brugmann University Hospital's clinical research unit included patients with PASC in the study. Whole blood samples were collected from 50 patients and 25 healthy volunteers. After stimulation under five different conditions, cytokine levels were measured using a multiplex method. Significantly decreased cytokine levels were observed in patients with PASC compared with healthy volunteers, particularly after TLR4 (interleukin [IL]-1, IL-1, IL-2, IL-10, interferon (IFN), IFN, IFN, and tumor necrosis factor (TNF)) and TLR7/8 (IL-1, IL-1, IFN, IFN, IFN, and TNF) pathway stimulation. Principal component analysis identified two distinct clusters, suggesting a likely dysregulation of immunity involving TLR4 and TLR7/8 pathways in patients with PASC. Our study suggests that TLR4 and TLR7/8 pathways play a role in the pathophysiology of PASC. Continuous basal activation of immunity could explain the high basal concentrations of cytokines described in these patients and the decreased amplitude of response of these signaling pathways following specific stimulation.

The widespread use of efficient vaccines against infectious diseases is regarded as one of the most significant advancements in public health and techniques for preventing and protecting against infectious diseases and cancer. Because the purpose of vaccination is to elicit an appropriate, powerful, and long-lasting immune response against the pathogen, compounds such as adjuvants must be used to enhance these responses. Adjuvants have been widely used since their discovery to boost immune responses, prevent diseases, and activate protective immunity. Today, several types of adjuvants with varying properties are available for specific applications. Adjuvants are supramolecular substances or complexes that strengthen and prolong the immune response to antigens. These compounds have long-term immunological effects and are low in toxicity. They also lower the amount of antigen or the number of immunogenic reactions needed to improve vaccine efficacy and are used in specific populations. This article provides an overview of the adjuvants commonly used in the vaccination industry, their respective mechanisms of action, and discusses how they function to stimulate the immune system. Understanding the mechanisms of action of adjuvants is crucial for the development of effective and safe vaccines.

The current study investigates COVID-19 infection likelihood using data from 5,819 respondents in Vietnam and Indonesia (December 10, 2022, to March 27, 2023) through binary logistic regressions. Descriptive statistics highlight the significance of vaccination status, with almost half of unvaccinated respondents contracting the infection. The second vaccine dose showed the lowest infection percentages, suggesting a potential dose-dependent effect. Those receiving mRNA vaccines consistently had reduced infection likelihood across the first four doses, with an unexpected reversal for the fifth dose. Vaccinated individuals, especially with mRNA vaccines, had faster recovery times, and variability in recovery times and milder symptoms were observed in mRNA vaccine recipients. Regression results from Model 1 reveal a substantial impact of vaccination, with vaccinated respondents having ∼48.1% lower odds than the unvaccinated. Model 2 underscores a dose-dependent protective effect, with each additional dose associated with a notable 6.6% reduction in infection likelihood. Beyond vaccination, gender, family size, marital status, employment, urban residence, and nationality influenced infection likelihood. Males, larger families, single marital status, unemployment, rural residence, and Indonesian nationality increased the likelihood of infection. Surprisingly, respondents with infected family members exhibited a lower infection likelihood, suggesting potential protective measures within households. These findings highlight COVID-19 dynamics, and ongoing research refines comprehension.

Global investment in developing COVID-19 vaccines has been substantial, but vaccine hesitancy has emerged due to misinformation. Concerns about adverse events, vaccine shortages, dosing confusion, mixing vaccines, and access issues contribute to hesitancy. Initially, the WHO recommended homologous vaccination (same vaccine for both doses), but evolving factors led to consideration of heterologous vaccination (different vaccines). The study compared reactogenicity and antibody response for both viral protein spike (S) and nucleocapsid (N) in 205 participants who received three vaccination regimens: same vaccine for all doses (Pfizer), two initial doses of the same vaccine (CoronaVac or AstraZeneca), and a Pfizer booster. ChAdOx1 and BNT162b2 vaccines were the most reactogenic vaccines, while CoronaVac vaccine was the least. ChAdOx1 and BNT162b2 achieved 100% of S-IgG seropositivity with one dose, while CoronaVac required two doses, emphasizing the importance of the second dose in achieving complete immunization across the population with different vaccine regimes. Pfizer recipients showed the highest S-IgG antibody titers, followed by AstraZeneca recipients, both after the first and second doses. A third vaccine dose was essential to boost the S-IgG antibodies and equalize the antibody levels among the different vaccine schedules. CoronaVac induced N-IgG antibodies, while in the Pfizer and AstraZeneca groups, they were induced by a natural infection, reinforcing the role of N protein as a biomarker of infection.

Aging is physiologically associated with a decline in the function of the immune system and subsequent susceptibility to infections. Interferon-gamma (IFN-), a key element in the activation of cellular immunity, plays an important role in defense against virus infections. Decreased levels of IFN- in the elderly may explain their increased risk for viral infectious diseases such as COVID-19. There is accumulating evidence that ascorbic acid (vitamin C [VitC]) and -tocopherol together help improve the function of the immune system in the elderly, control infections, and decrease the treatment duration. A SARS-CoV-2 strain was isolated from a patient and then cultured in the Vero cell line. The isolated and propagated virus was then inactivated using formalin and purified by the column chromatography. The inactivated SARS-CoV-2 was formulated in the Alum adjuvant combined with VitC or -tocopherol and/or both of them. The vaccines were injected twice to young and aged C57BL/6 mice. Two weeks later, IFN-, IL-4, and IL-2 cytokines were assessed using ELISA Kits. Specific IgG and IgG1/IgG2a were assessed by an in-house ELISA. In addition, the expression of PD1 and genes in the spleen tissue of the mice was measured using real-time PCR. IL-4 and IFN- cytokines showed a significant increase in both aged and young mice compared with the Alum-based vaccine. In addition, our results exhibited a significant decrease and increase in specific total IgG and the IgG2a/IgG1 ratio, respectively. Furthermore, the vaccine formulated in -tocopherol + VitC led to decreased PD1 and increased gene expression levels. In conclusion, our results demonstrated that -tocopherol + VitC formulated in the inactivated SARS-CoV-2 vaccine led to a shift toward Th1, which may be due to their effect on the physiology of cells, especially aged ones and changing their phenotype toward young cells.

It is difficult to differentiate between coronavirus disease 2019 (COVID-19) and influenza based on the symptoms. In the present study, a newly developed antigen rapid diagnostic test (Ag-RDT) called Panbio™ COVID-19/Flu A&B that can simultaneously detect severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and influenza A/B virus was evaluated. Its accuracy was evaluated using 235 pairs of nasopharyngeal samples collected from patients with respiratory symptoms and fever (>37.5°C). Reverse transcription polymerase chain reaction was used as a reference method to evaluate the accuracy of the SARS-CoV-2 detection. We confirmed the accuracy of the developed Ag-RDT against the Omicron variant where the sensitivity and specificity were 94.8% and 100%, respectively. In addition, to identify the influenza A virus, a noninferiority test was conducted using a commercial Ag-RDT, which has a sensitivity and specificity in comparison with viral culture of 94.8% and 98.4%, respectively. The positive and negative predictive values for influenza A virus were 98.5% and 98.1%, respectively, for the Panbio COVID-19/Flu A&B test. The evaluation of this newly developed Ag-RDT using clinical samples suggests that it has a high efficacy in clinical settings.

The hepatitis B virus (HBV) chronic infection goes through different phases, i.e., immune tolerant (IT), immune clearance (IC), and inactive carrier (IN) resulting from the interplay of viral replication and immune response. Although the adaptive immune response is central to viral control, roles of the innate immune cells are less prominent. We explored monocyte transcriptome in these different phases of HBV infection to understand the nature of its involvement and identify unique differentially expressed genes (DEGs) in each phase. CD14+ peripheral blood monocytes were isolated from patients in the IT, IC, and IN phases and from healthy subjects and their RNA was sequenced. The significant DEGs were studied through gene annotation databases to understand differentially modulated pathways. The DEGs were further validated by qRT-PCR to identify genes that were uniquely expressed in each phase. It was found that was upregulated in all the HBV samples. The IN phase had six uniquely upregulated genes, i.e., and . was most consistently downregulated in the IT phase, and in the IC phase, and were specifically downregulated. Cut-off values were generated by ROC curve analysis to differentiate between the groups based on their expression levels. The monocyte functions are majorly suppressed in the IT and IC phases and are, however, somewhat metabolically active in the IN phase.

To develop polyomavirus VP1 recombinant protein-based immunoassay, the expression of two polyomavirus (Karolinska Institute Polyomavirus; KIPyV, and Washington University Polyomavirus; WUPyV) VP1s in insect cells was investigated using an improved baculovirus system (BacMagic). The reliability of the purified VP1 to serve as antigens in serological tests was confirmed by the establishment of an enzyme-linked immunosorbent assay (ELISA). Two panels of serum samples were used, with Panel I comprising 60 sera (20 KIPyV-positive, 20 WUPyV-positive, and 20 negative) and Panel II consisting of 134 sera with unknown status. The seroprevalence of KIPyV and WUPyV in the study population was determined to be 62% and 50%, respectively. Antibody-negative sera exhibited low reactivities in both ELISAs, whereas antibody-positive sera displayed high reactivity with median optical density values of 1.37 and 1.47 in the KIPyV and WUPyV ELISAs, respectively. The differences in seroreactivities between antibody positive and negative for each virus were statistically significant ( < 0.0001; with 95% confidence interval). The study suggests that seroconversion for KIPyV and WUPyV occurs in childhood, with KIPyV seropositivity reaching 70% and WUPyV seropositivity reaching 60% after the age of 5 years. Adult seroprevalence for polyomaviruses was high, with more than 64% and 51% of the adult population being seropositive for KIPyV and WUPyV, respectively. The constant prevalence of KIPyV and WUPyV antibody in the age groups suggested that this antibody persists for life. The fact that antibody titers were generally stable over time revealed a persistent infection of polyomaviruses in the human population. The insect cell-derived recombinant VP1-based ELISA has been demonstrated to be valuable as a serological assay, offering a valid, reliable, fast, nonlaborious, and economical procedure.

The COVID-19 pandemic response has been hindered by the absence of an efficient antiviral therapy for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The reason why the previous preventative approach to COVID-19 solely through vaccines has failed could be a lack of understanding of how quickly the SARS-CoV-2 virus evolves. Given the absence of specific treatments for the virus, efforts have been underway to explore treatment options. Drug repurposing involves identifying new therapeutic uses for approved drugs, proving to be a time-saving strategy with minimal risk of failure. In this study, we report the successful use of a multidrug approach in patients with COVID-19. Successful administration of multidrug therapy, such as combinations of hydroxychloroquine and azithromycin, doxycycline and ivermectin, or ivermectin, doxycycline, and azithromycin, has been reported. Multidrug therapy is effective because of the differing mechanisms of action of these drugs, and it may also mitigate the emergence of drug-resistant SARS-CoV-2 strains. The medicines were lopinavir/ritonavir (Kaletra), bamlanivimab (monoclonal antibody), glycopyrrolate-formoterol (Bevespi), ciclesonide (Alvesco), famotidine (Pepcid), and diphenhydramine (Benadryl).

Human papillomavirus (HPV) is a circular, double-stranded DNA virus and recognized as the most prevalent sexually transmitted infectious agent worldwide. The HPV life cycle encompasses three primary stages. First, the virus infiltrates the basal cells of the stratified epidermis. Second, there is a low-level expression of viral genes and preservation of the viral genome in the basal layer. Lastly, productive replication of HPV occurs in differentiated cells. An effective immune response, involving various immune cells, including innate immunity, keratinocytes, dendritic cells, and natural killer T cells, is instrumental in clearing HPV infection and thwarting the development of HPV-associated tumors. Vaccines have demonstrated their efficacy in preventing genital warts, high-grade precancerous lesions, and cancers in females. In males, the vaccines can also aid in preventing genital warts, anal precancerous lesions, and cancer. This comprehensive review aims to provide a thorough and detailed exploration of HPV infections, delving into its genetic characteristics, life cycle, pathogenesis, and the role of high-risk and low-risk HPV strains. In addition, this review seeks to elucidate the intricate immune interactions that govern HPV infections, spanning from innate immunity to adaptive immune responses, as well as examining the evasion mechanisms used by the virus. Furthermore, the article discusses the current landscape of HPV vaccines and common treatments, contributing to a holistic understanding of HPV and its associated diseases.

Cytomegalovirus (CMV) has long been thought to have an association with glioblastoma multiforme (GBM), although the exact role of CMV and any subsequent implications for treatment have yet to be fully understood. This study addressed whether IGH complementarity determining region-3 (CDR3)-CMV protein chemical complementarity, with IGH CDR3s representing both tumor resident and blood-sourced recombinations, was associated with overall survival (OS) distinctions. recombination sequencing reads were obtained from (a) the Clinical Proteomic Tumor Analysis Consortium, tumor RNAseq files; and (b) the cancer genome atlas, blood exome-derived files. The Adaptive Match web tool was used to calculate chemical complementarity scores (CSs) based on hydrophobic interactions, and those scores were used to group GBM cases and assess survival probabilities. We found a higher OS probability for cases whose hydrophobic IGH CDR3-CMV protein chemical complementarity scores (Hydro CSs) were in the upper 50th percentile for several CMV proteins, including UL99 and UL123, as well as for CSs based on known B cell epitopes representing these proteins. We also identified multiple immune signature genes, including CD79A and TNFRSF17, for which higher RNA expression was associated with higher Hydro CSs. Results were consistent with the idea that stronger immunoglobulin responses to CMV are associated with better OS probabilities for GBM.