Abstract
Background and aims
Adenoviral pneumonia is a significant cause of morbidity and mortality among children. There is limited data about the clinical profile, intensive care needs, and outcomes of children with adenoviral pneumonia from resource-limited settings.
Patients and methods
This retrospective study was conducted in the pediatric emergency room (PER) and pediatric intensive care unit (PICU) of a tertiary care hospital in North India over a period of a period of 2 years (July 2022 to June 2024). The data collection included demographic and clinical features, laboratory investigations, complications, treatment, intensive care needs, and outcomes.
Results
Eighty-five children were enrolled, majority were <1 year of age and males (71.7% each). All presented with fever and respiratory symptoms. The common complications were acute respiratory distress syndrome (ARDS) (47%), multiple organ dysfunction syndrome (MODS) (26%), shock (25%), and encephalopathy (25%). PICU admission was needed in 46% of children. The intensive care needs included invasive mechanical ventilation (48%), CPAP (39%), HFNC (9%), vasoactive drugs (25%), IVIG (8%), RRT (6%), and cidofovir (5%). The duration of ER, PICU, and hospital stay was 48 (24–96) hours, 7 (4–14) days, and 9 (5–18) days, respectively. The mortality rate was 22%. On multivariate analysis, the independent predictors of mortality were low admission pH, myocardial dysfunction, acute kidney (AKI), ARDS, shock, encephalopathy, MODS, and healthcare-associated infection (HCAI).
Conclusion
Infants constituted the largest group of patients requiring admission for adenoviral infection to pediatric emergency in a tertiary care center. Common complications were ARDS, shock, MODS, and encephalopathy. Nearly half required PICU admission for organ support. The mortality rate was 22%; and low admission pH, myocardial dysfunction, AKI, ARDS, shock, encephalopathy, MODS, and HCAI were independent predictors of mortality.
How to cite this article
Vyasam S, Jayaram J, Sarkar S, Angurana SK, Raj S, Bora I, et al. Clinical Profile, Intensive Care Needs, and Outcome of Children with Adenoviral Pneumonia: A Retrospective Study from a Tertiary Care Hospital in North India. Indian J Crit Care Med 2025;29(7):586–591.
Keywords: Acute respiratory distress syndrome, Adenovirus, Cidofovir, Multiple organ dysfunction syndrome, Pediatric intensive care unit
Highlights
Infants constituted the largest group of patients requiring admission for adenoviral infection to pediatric emergency in a tertiary care center.
Common complications were acute respiratory distress syndrome (ARDS), shock, multiple organ dysfunction syndrome (MODS), and encephalopathy.
PICU admission was needed in nearly half of the children and the mortality rate was 22%.
Low admission pH, myocardial dysfunction, acute kidney (AKI), ARDS, shock, encephalopathy, MODS, and healthcare-associated infection (HCAI) were independent predictors of mortality.
Introduction
Globally, human adenovirus is a leading cause of respiratory illnesses in children, accounting for approximately 5–10% of childhood pneumonia, with higher prevalence in those under five years of age.1–3 While most infections are mild and self-limiting, 1/3rd of cases develop severe pneumonia requiring intensive care and are associated with significant morbidity and mortality, particularly in resource-limited settings like India.1,2,4–6 After the COVID-19 pandemic, there has been an increase in adenoviral pneumonia among children.1–3,7
Recent studies have identified adenovirus as a significant pathogen in pediatric intensive care units (PICUs), with clinical presentations ranging from mild upper respiratory tract infections to severe pneumonia, acute respiratory distress syndrome (ARDS), encephalopathy, and multiorgan dysfunction syndrome (MODS).1–3,7,8 Understanding the clinical characteristics and risk factors associated with poor outcomes in children with adenoviral pneumonia is crucial for early recognition and appropriate management. Previous studies have suggested that factors such as age, underlying comorbidities, development of complications, liver dysfunction, and healthcare-associated infections (HCAIs) were potential predictors of mortality.8–10 However, most of these studies are from developed countries, and their findings may not be directly applicable to resource-limited settings. Moreover, there is limited data from Indian settings regarding the clinical profile, complications, intensive care needs, and outcomes of children with adenoviral pneumonia.
Therefore, we planned this retrospective study to describe the clinical profile, complications, intensive care needs, outcomes, and predictors of mortality of children with adenoviral pneumonia admitted to the pediatric emergency room (PER) and PICU of a tertiary care hospital in North India.
Patients and Methods
This retrospective study was conducted in the PER and PICU of a tertiary care teaching hospital in North India over a period of 2 years (July 2022 to June 2024). The study protocol was approved by the Institute Ethics Committee and the manuscript was approved by the Departmental Review Board.
Children aged 1 month to 12 years with confirmed adenoviral pneumonia (positive nasopharyngeal swab for adenovirus by RT-PCR) and requiring admission to the ER or PICU were included. Data was collected from admission files and an electronic hospital database on a pre-structured data collection proforma. The data regarding demographic details (age, gender), clinical features, presence of underlying comorbidities, laboratory parameters, complications and organ dysfunction, treatment, PICU admission, and intensive care needs (mechanical ventilation, vasoactive drugs, blood products, and renal replacement therapy) was collected. The duration of PER, PICU, and hospital stay were noted. The outcome included survival or mortality.
Acute respiratory distress syndrome was defined according to the Pediatric Acute Lung Injury Consensus Conference (PALICC-2) 2023 criteria.11 Multiorgan dysfunction syndrome is defined as the dysfunction of two or more organ systems. The shock was defined as per the Surviving Sepsis Campaign Guidelines.12 Acute kidney was defined using the KDIGO criteria.13 Healthcare-associated infections were defined according to CDC/NHSN surveillance definitions.14
All patients were managed according to standard unit protocols. This included respiratory support (oxygen therapy, noninvasive or invasive mechanical ventilation as required), fluid management and vasoactive support, antimicrobial, and antiviral therapy (if indicated), and other organ supportive care.
The primary outcome was mortality rate and secondary outcomes were clinical profile, intensive care needs, and predictors of mortality among children with adenoviral pneumonia.
Data were analyzed using [IBM SPSS Statistics V.29]. Continuous variables were expressed as median (interquartile range) and categorical variables were expressed as frequencies and percentages. Univariate analysis was performed using the Mann–Whitney U test for continuous variables and Chi-square or Fisher's exact test for categorical variables. Multivariate logistic regression analysis was performed to identify independent predictors of mortality. A p-value < 0.05 was considered statistically significant.
We planned to enroll all consecutive children admitted with adenoviral pneumonia to PER and PICU during the study period of 2 years.
Results
A total of 85 children with adenoviral pneumonia were enrolled. The majority of children were below 1 year of age (71.7%, n = 61) and with a male predominance (71.7%, n = 61). All children had fever and respiratory symptoms. Neurological and gastrointestinal symptoms were observed in 31.8% (n = 27) of children each. More than half of the children (54.1%) had respiratory failure at presentation. Underlying comorbidities were noted in 22.4% (n = 19) children with congenital cardiac disease and neurological/neuromuscular disease in 5.9% (n = 5) each; and suspected immunodeficiency and acute leukemia in 3.5% (n = 3) children each (Table 1).
Table 1.
Baseline characteristics of children with adenoviral pneumonia
| Category | Total cases, n = 85 |
|---|---|
| Male, n (%) | 61 (71.7) |
| Age-groups (years), n (%) | |
| <1 | 61 (71.7) |
| 1–5 | 17 (20) |
| 6–10 | 4 (4.7) |
| >10 | 3 (3.5) |
| Clinical features, n (%) | |
| Fever | 85 (100) |
| Respiratory symptoms | 85 (100) |
| Neurological symptoms | 27 (31.8) |
| Gastrointestinal symptoms | 27 (31.8) |
| Renal symptoms | 3 (3.5) |
| Presented in respiratory failure, n (%) | 46 (54.1) |
| Underlying comorbidities, n (%) | 19 (22.4) |
| Congenital cardiac disease | 5 (5.9) |
| Neurological/neuromuscular disease | 5 (5.9) |
| Suspected immunodeficiency | 3 (3.5) |
| Acute leukemia | 3 (3.5) |
| Chronic lung disease | 2 (2.4) |
| Neonatal ventilation | 1 (1.2) |
Laboratory abnormalities included elevated C-reactive protein (CRP) (56.5%), anemia (28.2%), transaminitis (22.3%), thrombocytopenia (18.8%), and hypernatremia (6.7%). The median (IQR) values of CRP and d-dimer were 31 (13–106) mg% and 3457 (2688-3922) ng/mL, respectively (Table 2). Among enrolled children, three had coinfection with adenovirus and RSV, while one had coinfection with adenovirus and bocavirus.
Table 2.
Laboratory investigations at admission and laboratory abnormalities in children with adenoviral pneumonia
| Laboratory parameter, median (Interquartile range) | Total cases, n = 85 |
|---|---|
| Hemoglobin (gm/%) | 9.7 (8.6–13) |
| Total counts (per cumm) | 8,200 (3,750–10,650) |
| Platelet counts (per cumm) | 219,000 (150,000–313,000) |
| C-reactive protein (CRP, mg%) | 32 (13–106) |
| Sodium (mEq/L) | 138 (135–141) |
| Potassium (mEq/L) | 4.6 (4.1.5) |
| Chloride (mEq/L) | 104 (102–108) |
| Urea (mg%) | 26 (19–44) |
| Creatinine (mg%) | 0.3 (0.3–0.5) |
| Serum glutamic oxaloacetic transaminase (SGOT, IU/L) | 79 (40–168) |
| Serum glutamic pyruvic transaminase (SGPT, IU/L) | 41 (22–87) |
| International normalized ratio (INR) | 1.2 (1.1–1.3) |
| d-Dimer (ng/mL) | 3457 (2688–3922) |
| Laboratory abnormalities, n (%) | |
| Elevated CRP | 48 (56.5) |
| Anemia | 24 (28.2) |
| Transaminitis | 19 (22.3) |
| Thrombocytopenia | 16 (18.8) |
| Hypernatremia | 6 (7.1) |
| Hyponatremia | 4 (4.7) |
| Hyperkalemia | 4 (4.7) |
| Hypokalemia | 4 (4.7) |
CRP, C-reactive protein
Organ dysfunction included ARDS (47.1%), MODS (25.9%), shock and encephalopathy (24.7% each), liver dysfunction (22.3%), acute kidney injury (AKI) (20%), thrombocytopenia (18.9%), and myocardial dysfunction (15.3%). These children received antimicrobials including ceftriaxone (41.2%), meropenem and vancomycin (21.2% each), ampicillin-gentamicin (16.5%), azithromycin (16.5%), colistin (8.2%), and oseltamivir (5.9%). Cidofovir was administered in only 4.7% (n = 4) of children. Seven (8.2%) children received intravenous immunoglobulin (IVIG) for myocardial dysfunction/myocarditis (Table 3).
Table 3.
Complications, organ supportive therapies, and outcome in children with adenoviral pneumonia
| Complications, n (%) | Total cases, n = 85 |
|---|---|
| Acute respiratory distress syndrome | 40 (47.1) |
| Multiorgan dysfunction syndrome | 22 (25.9) |
| Shock | 21 (24.7) |
| Encephalopathy | 21 (24.7) |
| Liver dysfunction | 19 (22.3) |
| Acute kidney Injury | 17 (20) |
| Thrombocytopenia | 16 (18.9) |
| Myocardial dysfunction | 13 (15.3) |
| Coagulopathy | 5 (5.9) |
| Antimicrobials, n (%) | |
| Ceftriaxone | 35 (41.2) |
| Meropenem | 18 (21.2) |
| Vancomycin | 18 (21.2) |
| Ampicillin/Gentamicin | 14 (16.5) |
| Azithromycin | 14 (16.5) |
| Colistin | 7 (8.2) |
| Oseltamivir | 5 (5.9) |
| Cidofovir | 4 (4.7) |
| Intravenous immunoglobulin, n (%) | 7 (8.2) |
| Organ supportive therapy, n (%) | |
| Pediatric intensive care unit admission | 39 (45.9) |
| Invasive mechanical ventilation | 41 (48.2) |
| Continuous positive airway pressure | 33 (38.8) |
| High-flow nasal cannula oxygen | 8 (9.4) |
| Noninvasive ventilation | 3 (3.5) |
| Central venous catheter | 35 (41.2) |
| Blood transfusion | 25 (29.4) |
| Vasoactive drugs | 21 (24.7) |
| Renal replacement therapy | 5 (5.9) |
| Healthcare-associated infections, n (%) | 12 (14.1) |
| Ventilator-associated pneumonia | 10 (11.8) |
| Bloodstream infection | 2 (2.3) |
| Duration, median (IQR) | |
| Duration of emergency room stay (hours) | 48 (24–96) |
| Duration of pediatric intensive care unit stay (days) | 7 (4–14) |
| Duration of hospital stay (days) | 9 (5–18) |
| Outcome, n (%) | |
| Survived | 66 (77.6) |
| Deaths | 19 (22.3) |
All cases were initially admitted to the ER, 45.9% (n = 39) were shifted to PICU, and 54.1% (n = 46) were managed in PER only. Organ supportive treatment included invasive mechanical ventilation (48.2%), CPAP (38.8%), central venous catheter placement (41.2%), blood/blood product transfusion (29.4%), vasoactive drugs (24.7%), and RRT (5.9%) (three peritoneal dialysis and two continuous renal replacement therapy). HCAIs were documented in 14.1% of children, with ventilator-associated pneumonia (11.8%) being the most common, followed by bloodstream infections (2.3%) (Table 3). The median (IQR) duration of PER, PICU, and hospital stay were 48 (24–96) hours, 7 (4–14) days, and 9 (5–18) days, respectively. The final outcomes were survival in 77.6% (n = 66), and mortality in 22.3% (n = 19) (Table 3). Among children admitted to PICU, the mortality rate was 33% (13/39), and among those who remained in PER, the mortality rate was 13% (6/46).
On univariate analysis, norsurvivors had significantly higher admission levels of urea, creatinine, serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase (SGPT), and CRP; and had lower pH. Also, complications such as anemia, transaminitis, myocardial dysfunction, AKI, coagulopathy, ARDS, shock, MODS, encephalopathy, and HCAIs were significantly associated with mortality. On multivariate logistic regression, lower admission pH; and presence of myocardial dysfunction, AKI, ARDS, shock, MODS, and HCAIs were independent predictors of mortality (Table 4).
Table 4.
Predictors of mortality in children with adenoviral pneumonia
| Patient characteristics | Survivors, n = 66 | Non-survivors, n = 19 | Univariate analysis | Multivariate analysis | ||
|---|---|---|---|---|---|---|
| OR (95% CI)/ Mann–Whitney U | p | OR (95% CI) | p | |||
| Age (years) | 0.6 (0.3–2) | 0.7 (0.3–2.3) | 385 | 0.328 | – | – |
| Males | 50 (75.8) | 8 (57.1) | 0.4 (0.2–1.4) | 0.192 | – | – |
| Duration of illness | 9 (5–19) | 14 (9.2–24.2) | 371 | 0.25 | – | – |
| Underlying comorbidity | 17 (25.8) | 4 (21.4) | 0.79 (0.2–3.26) | 1 | – | – |
| PICU admission | 28 (42.4) | 10 (52.6) | 3.39 (1–11.9) | 0.08 | – | – |
| Hemoglobin | 9.7 (8.7–13.7) | 9.6 (8.3–13.8) | 64.5 | 0.599 | – | – |
| TLC | 8,300 (8,750–10,700) | 5,600 (8,300–10,100) | 114 | 0.619 | – | – |
| Platelet counts | 2,14,500 (1,50,750–3,20,750) | 2,00,000 (1,40,000–2,35,250) | 371 | 0.316 | – | – |
| Urea | 24 (18–33) | 55 (23–97) | 208.5 | 0.002 | 1.1 (0.3–3.2) | 0.99 |
| Creatinine | 0.3 (0.2–0.4) | 0.8 (0.4–1.8) | 201 | 0.001 | 1.55 (0.5–4.5) | 0.42 |
| SGOT | 62 (37–144) | 152 (60–1068) | 267.5 | 0.022 | 1.0006 | 1 |
| SGPT | 33 (20–56) | 49 (37–527) | 265 | 0.02 | 1.0005 | 1 |
| CRP | 24 (10–83) | 114 (57–162) | 110 | 0.001 | 1.001 | 1 |
| INR | 1.2 (1.1–1.3) | 1.2 (1.1–1.8) | 146 | 0.329 | ||
| D dimer | 3283 (2509–3800) | 3696 (2831–5942) | 26 | 0.254 | ||
| pH | 7.3 (7.3–7.4) | 7.3 (7.3) | 232 | 0.004 | 0.5 (0.4–0.6) | <0.05 |
| Bicarbonate | 24 (21–26) | 22 (20-25) | 344 | 0.152 | – | – |
| Anemia | 14 (21.2) | 8 (42.1) | 4.95 (1.4–16) | <0.05 | 1.31 (0.5–3.2) | 0.55 |
| Liver dysfunction | 10 (15.2) | 7 (37) | 5.6 (1.6–19) | <0.05 | 1.6 (0.7–3.6) | 0.26 |
| Thrombocytopenia | 9 (13.6) | 5 (36) | 3.5 (1–13) | 0.063 | – | – |
| Myocardial dysfunction | 4 (6.1) | 9 (47.3) | 28 (6–123) | <0.05 | 2.1 (1–4.2) | 0.05 |
| AKI | 4 (6.1) | 11 (58) | 57 (11–289) | <0.05 | 2.5 (1.2–5.4) | 0.02 |
| Coagulopathy | 1 (1.5) | 3 (16) | 17.7 (1.6–186) | <0.05 | 1.1 (0.–1.6) | 0.77 |
| ARDS | 23 (34.8) | 19 (100) | – | <0.05 | 6.4 (3.1–13) | <0.05 |
| Shock | 6 (9.1) | 19 (100) | – | <0.05 | 3.7 (1.6–8.8) | <0.05 |
| MODS | 6 (9.1) | 17 (93) | 130 (14–1173) | <0.05 | 3.8 (1.7–8.9) | <0.05 |
| Encephalopathy | 8 (12.1) | 12 (64) | 13 (3.5–48) | <0.05 | 1.3 (0.6–3) | 0.48 |
| HCAI | 7 (10.6) | 5 (27) | 4.68 (1.2–18) | <0.05 | 7.5 (2.3–24) | <0.05 |
Bold text indicate significant p-values. AKI, acute kidney injury; ARDS, acute respiratory distress syndrome; CI, confidence interval; CRP, C-reactive protein; HCAI, healthcare-associated infection; INR, international normalized ratio; MODS, multiorgan dysfunction syndrome; OR, odds ratio; PICU, pediatric intensive care unit; SGOT, serum glutamic oxaloacetic transaminase; SGPT, serum glutamic pyruvic transaminase; TLC, total leukocyte count
Discussion
Adenoviral pneumonia remains a major cause of morbidity and mortality, particularly in young children, with greater impact among those with severe disease requiring intensive care, especially in resource-limited settings.1–3 Recent studies demonstrated that adenovirus contributed to nearly 25% of children admitted to PICU with respiratory viral infections and associated with high mortality.3,7,15 In the post-COVID-19 pandemic period, there has been a paradigm shift in the epidemiology, clinical presentation, and severity patterns of respiratory viral infections with increased occurrence of pneumonia due to adenovirus among children.1–3,7,16–24
The predominance of a high proportion of infants (71.7%) aligns closely with findings of previous studies,1,2,7,10,25 which highlights the vulnerability of younger children to severe adenoviral infections, likely due to their immature immune systems and limited adaptive immunity.4,7
The most common complications noted were ARDS (47.1%), MODS (25.9%), shock (24.7%), encephalopathy (24.7%), liver dysfunction (22.3%), and AKI (20%). The high prevalence of severe pulmonary and extrapulmonary complications in the index cohort mirrors the patterns observed in recent studies of adenoviral respiratory infections among children.1,2,10,26–28 Varadarajan et al.1 reported similar rates of complications in children with adenoviral pneumonia (ARDS 42%, MODS 23%, shock 28%). Bera et al.2 highlighted that ARDS was a key complication in a series of children with severe acute respiratory infections due to adenovirus. The high prevalence of these complications reflects the respiratory tropism of adenovirus and its potential to cause severe pulmonary injury, systemic inflammation, and multiorgan dysfunction.1,2,10 Neurological complications, particularly encephalopathy were noted in 24.7% of children in index study, which is much higher than the usual reported rates of neurological complications in adenovirus infection among children (<2%).28,29 Higher rate of pulmonary and extrapulmonary complications emphasizes the need for vigilant monitoring and prompt intervention to treat these complications.
The intensive care needs in the index study showed similarities with findings by Varadarajan et al.1 in terms of invasive mechanical ventilation (48.2% vs 45%), central line placement (41.2% vs 38%), and blood transfusion (29.4% vs 32%). These comparable rates suggest consistent patterns of intensive care needs, organ support requirements, and resource utilization in severe adenovirus infections across Indian tertiary care centers.1,2,21
Although there is some evidence that cidofovir reduces adenovirus load and improves survival, it has not been widely used in children and there are no established clinical guidelines for the use of cidofovir in children with adenoviral pneumonia.8 We started using cidofovir in mid-2024 and it was used in four cases (4.7%). Due to limited availability, financial issues, and no clear-cut guidelines, not all children with adenoviral pneumonia received cidofovir. In the index study, IVIG was used in children with myocardial dysfunction/myocarditis. (n = 7, 8.2%) based on the severity of the disease and hemodynamic status. As this was a retrospective study, the usage of cidofovir and IVIG was guided by the availability at that point of time cost factor/affordability (for cidofovir), and discretion of the treating pediatric intensivist.
The mortality rate in index study was 22.3% which is higher than reported mortality rates in Indian studies (12–15.8%) and global figures (8–12%) among children admitted in PICU with adenovirus infection.1,2,9,10 These findings highlight that there is a substantial burden of adenoviral pneumonia among critically ill children in India. The higher mortality in Indian settings may be attributed to delayed presentations, resource limitations, or differences in healthcare infrastructure. The mortality in the PICU and ER cohorts was 33% and 13%, respectively. This suggested that the majority of cases with severe disease were managed in PICU and had higher mortality than those who remained in PER.
The pattern of extrapulmonary complications and mortality aligns with a recent study from our unit involving children admitted with non-COVID-19 severe acute respiratory infections during the COVID-19 pandemic.16 This parallel trend suggests a broader pattern of severe viral respiratory infections in children during the pandemic and in the postpandemic era. Postpandemic, in addition to an increase in respiratory infections due to adenovirus among critically ill children, other viral pathogens like human metapneumovirus and bocavirus have been reported to cause multisystem involvement and severe complications.22,30
Univariate analysis demonstrated that norsurvivors had significantly higher levels of urea, creatinine, SGOT, SGPT, and CRP; had lower pH; and higher rates of anemia, liver dysfunction, myocardial dysfunction, AKI, coagulopathy, ARDS, shock, MODS, encephalopathy, and HCAIs. These findings suggest that multiorgan dysfunction plays a critical role in the progression of severe adenoviral infection. Elevated CRP levels, indicative of systemic inflammation, have been associated with severe disease and poor outcomes in adenoviral pneumonia.31,32 Multivariate logistic regression demonstrated that lower admission pH; and presence of myocardial dysfunction, AKI, ARDS, shock, liver dysfunction, MODS, and HCAIs were independent predictors of mortality. These findings are consistent with previous studies where AKI, shock, MODS, and HCAIs were significant predictors of mortality in adenovirus infection.1,2,8–10
HCAIs were documented in 14.1% of children in the index study comparable to other studies from India (10%),1,2 reflecting variations in infection control practices, longer PICU stay, and need for mechanical ventilation in these children. This finding has relevance in resource-limited settings where HCAIs burden remains substantial highlighting the urgent need for robust infection prevention strategies in intensive care settings.
The strengths of this study include a comprehensive analysis of clinical and laboratory data, complications, intensive care needs, and outcomes, among children with adenoviral pneumonia. The use of standardized definitions ensured consistency and reliability in the findings. The independent predictors of mortality were identified, contributing to a deeper understanding of factors influencing patient outcomes. The limitations of this study include a single-center design with limited generalizability of the findings to other clinical settings. There is a lack of long-term outcomes leaving gaps in the understanding of the extended impact of adenoviral pneumonia. As a tertiary care center, there may be a potential for referral bias, which could have influenced the study results.
Conclusion
Infants constituted the largest group of patients requiring admission for adenoviral infection to pediatric emergency in a tertiary care center. Common complications noted were ARDS (47%), MODS (26%), shock (25%), liver dysfunction (22%), and AKI (20%). Nearly half of children required PICU admission for organ support. Lower admission pH; and presence of myocardial dysfunction, AKI, ARDS, shock, MODS, and HCAIs were independent predictors of mortality.
IEC Approval
IEC approval was obtained from the IEC (intramural), PGIMER, Chandigarh. Letter no.: INT/IEC/2023/SPL-1022A dated 21/11/2023.
Author Contribution
SV, data collection, data analysis, literature review, and manuscript preparation. JJ, data collection, literature review, and data analysis. SS, data collection, virological investigations, and review of manuscript. SKA, conceptualized the study, supervised data collection and data analysis, and reviewed the manuscript. SR, data analysis. IB, Data collection, virological investigations, and review of manuscript. KN, supervised data analysis and reviewed the manuscript. AB, supervised data collection and reviewed the manuscript. JM, conceptualized the study designs and reviewed the manuscript. RKR, conceptualized the study designs, supervised virological investigations, and reviewed the manuscript.
Acknowledgment
The authors thank the Regional Virus Research and Diagnostic Laboratory (RVRDL), Department of Health Research, Ministry of Health and Family Welfare (MoHFW), Government of India, for providing infrastructure and consumables to carry out the study.
Orcid
Siva Vyasam https://orcid.org/0000-0002-0887-1535
Jyothi Jayaram https://orcid.org/0009-0007-0377-4625
Subhabrata Sarkar https://orcid.org/0000-0001-8880-8458
Suresh Kumar Angurana https://orcid.org/0000-0001-6370-8258
Shubham Raj https://orcid.org/0000-0002-4998-4632
Ishani Bora https://orcid.org/0000-0002-7573-3300
Karthi Nallasamy https://orcid.org/0000-0002-6713-9846
Arun Bansal https://orcid.org/0000-0001-6212-6889
Jayashree Muralidharan https://orcid.org/0000-0002-6149-1355
Radha K Ratho https://orcid.org/0000-0001-7205-9325
Footnotes
Source of support: Nil
Conflict of interest: None
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