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With the invention of the stethoscope, in the early 1800s, a better diagnosis of heart and lung disorders was opened up. Through the stethoscope's 200-year history, there has been a significant development of the stethoscopy from the use of the simple monaural earpiece to the binaural stethoscope, followed by the electronic stethoscope, which, together with other studies, has enabled a thorough diagnosis of these disorders. Here is a glimpse of this story. The cross-border investigation Far back in time, it has been clear that the function of the heart and lungs played an important role in maintaining life. By tapping with the finger (percussion) and putting the ear to the patient's chest (auscultation), it could hear sound from the body telling about the patient's condition, especially about the presence of fluid or air-filled organs. Auscultation is already described in the Corpus Hippocraticum, in the Diseases II section [1]. The doctor puts the ear to the chest of a patient with water sores, to hear the pain as a wine vinegar from the lungs - or the doctor grabs the patient about the shoulders, shakes him and places his ear to his chest to hear in which side his pleuritis is sitting. Since then, auscultation seems to have been partially forgotten, although it has probably been known by Ambroise Paré and William Harvey [2]. It was not until the late 1700s that it became an important diagnostic aid, just like the pulse clock and the medical thermometer [3 p. 277]. Here, Joseph Leopold Auenbrugger (1722-1809) is considered to be the father of the modern physical examination, which is based on percussion. Percussion he performed by knocking direcly on the thorax with the finger or cupped hands. His discovery of the percussion sounds from the chest during inhaling and exhaling originates from his work in 1760 at the Vienna Military Hospital [4]. In 1761, His little book on thoracic percussion revealing thoracic diseases appeared in 1761 [3p.271], which in 1808 was translated into French by the Parisian physician Jean Nicolas Corvisart des Marets (1755-1821). This contributed to the French doctors starting to use percussion and ausculation more routinely [5]. The limitation of simple auscultation was the fact that the sound was weak and incomplete and therefore there was a need for improved sound quality. In addition, the direct contact with the patient's body could seem insulting

Asthma is a highly prevalent airway disease with multiple phenotypes [1,2]. Adult-onset eosinophilic asthma is a severe asthma subtype associated with more frequent and severe exacerbations, the development of persistent airflow limitation and a poorer quality of life. This type of asthma is much more difficult to control than other asthma subtypes, requiring high doses of inhaled or even oral corticosteroids (OCS) [3,4]. Recently, several new monoclonal antibody therapies have been approved for eosinophilic severe asthma, including anti-IL-5 treatment. IL-5 is essential for eosinophilic maturation and survival [5] and anti-IL5 treatment has markedly reduced asthma exacerbations with sparing of OCS use in patients with eosinophilic asthma [6]. Eosinophilic asthma is frequently associated with chronic rhinosinusitis and/or nasal polyposis [7], suggesting that a similar eosinophilic inflammatory process might drive both conditions. Eosinophilic otitis media (EOM) also might fit in this concept, showing remarkable similarities with asthma and nasal polyposis. The disease was first reported in 1994, but only since 2011 diagnostic criteria for EOM were identified. If a patient shows otitis media with effusion or chronic otitis media with eosinophil-dominant effusion (major criterion) and is being positive for ≥2 items of the 4 minor criteria (highly viscous middle ear effusion, resistance to conventional treatment, association with asthma, association with nasal polyposis) he is diagnosed as having EOM. Eosinophilic granulomatosis with polyangiitis and hypereosinophilic syndrome must be excluded [8].

Objective: Dysfunctional breathing (DB) refers to abnormal patterns of breathing. No gold standard exists for diagnosis. In clinical practice we regularly see children with functional breathing problems. We collected data from this patient group to gain more insight into the characteristics of children with dysfunctional breathing. Methods: We composed a retrospective, cross-sectional study. The population consisted of children referred to a physiotherapist by a pediatrician due to suspected dysfunctional breathing. Data from 2013-2015 were collected from patient files, selected according to patterns and onset of symptoms, concomitant asthma, Nijmegen questionnaire (NQ) score, maximum exercise capacity and breathing pattern. Results: A total of 201 patients were included in the study, 66% of whom were female. The mean age was 13.9 years; 26% of the children were overweight. The most frequently reported symptoms were breathlessness, chest pain/tightness and dizziness. Fifty-two percent had a NQ score ≥23, mainly female. Twenty-eight percent of the children scored < p5 for their age on maximum exercise capacity; this proportion was substantially higher among males. Of the total population, 78% scored < p50 for their age. Subgroups with a higher body mass index (BMI) showed lower maximum exercise capacity. Children presenting with pulmonary symptoms were primarily misdiagnosed with asthma. Conclusion: Dysfunctional breathing is a common cause of respiratory complaints. Most children with dysfunctional breathing have a high BMI and are in poor physical condition, which suggests a clinically relevant comorbidity and possible options for therapy. Children are often falsely diagnosed with asthma; better recognition will decrease unnecessary medication use.Introduction

Introduction: The disease outbreak of COVID-19 has had a great clinical and microbiological impact in the last few months. In the preanalytical phase, the collection a sample from of a respiratory tract at the adequate moment and from the correct anatomical site is essential for a rapid and precise molecular diagnosis with a false negative rate of less than 20%. Materials and methods: We conducted a descriptive study of COVID-19 disease with a persistently negative RT-PCR test in patients seen at the National Institute of Respiratory Diseases (INER) in Mexico City in the period of March through May of 2020. 38 patients were registered with negative RT-PCR test obtained through nasopharyngeal and oropharyngeal swabbing. We evaluated the distribution of data with the Shapiro-Wilk test of normality. The non-parametric data are reported with median. The nominal and ordinal variables are presented as percentages. Results: The average age of our cohort was 46 years and 52.63% were male (n = 20). Diabetes Mellitus was documented in 34.21% (n = 13) of the patients, Systemic Hypertension in 21.05% (n = 8), Obesity in 31.57% (n = 12) and Overweight in 42.10% (n = 16). Exposure to tobacco smoke was reported in 47.36% (n = 18) of the patients. The median initial saturation of oxygen was 87% at room air. The severity of the disease on admission was: mild 71.05% (n = 27), moderate 21.05% (n = 8) and severe or critical in 7.89% (n = 3) of the cases respectively. 63.15% (n = 24) sought medical care after 6 or more days with symptoms. Lymphopenia was documented in 78.94% (n = 30). Median LDH at the time of admission was 300, being elevated in 63.15% (n = 24) of the cases. The initial tomographic imaging of the chest revealed predominantly ground glass pattern in 81.57% (n = 31) and predominantly consolidation in 18.42% (n = 7). The registered mortality was 15.78% (n = 6). Conclusion: Patients with COVID-19 and a persistently negative RT-PCR test with fatal outcomes did not differ from the rest of the COVID-19 population since they present with the same risk factors shared by the rest of patients like lymphopenia, comorbidities, elevation of D-Dimer and DHL on admission as well as a tomographic COVID-19 score of severe illness, however we could suggest that the percentage of patients with a mild form of the disease is higher in those with a persistently negative RT-PCR test.

Objective: To assess the knowledge, attitudes and practices declared among general practitioners (GPs) concerning the use of antibiotics for the treatment of ARI in children under 5 years in Lubumbashi. Methods: A cross-sectional survey was conducted to assess the level of knowledge, attitude and practices concerning antibiotic prescribing among 67 GPs working in the pediatric setting in various health structures in Lubumbashi city, in the Democratic Republic of Congo. Data were collected from April 1st to June 30th, 2020. Results: GPs had limited knowledge about antibiotic prescriptions (mean of 46% correct answers to 8 questions). Although they are generally concerned about antibiotic resistance (mean ± SD = 0.50 ± 0.68), and are unwilling to submit to pressure to prescribe antibiotics to meet patient demands and expectations (mean ± SD = –1.78 ± 0.31) and the requirements to prescribe antibiotics for fear of losing patients (mean ± SD = –1.67 ± 0.47), there was a lack of motivation to change prescribing practices (mean ± SD = −0.37 ± 0.94) and strong agreement that they themselves should take responsibility for tackling antibiotic resistance (mean ± SD = 1.24 ± 0.74). Multiple linear regression results showed that higher knowledge scores were associated with less avoidance of responsibility when prescribing antibiotics (β = 0.919; p = 0.000). Conclusion: To curb the over-prescription of antibiotics, it is not enough to improve knowledge in itself. The lack of motivation of physicians to change must be addressed through a systematic approach. These data show the need for interventions that support the rational prescribing of antibiotics.

Spontaneous pneumomediastinum (SPM) is a rare condition, more commonly seen in patients with history of asthma, chronic obstructive pulmonary disease, infections, or drug users. Today, we face one novel virus that has cause an outbreak of acute respiratory illness, affecting over a million individuals worldwide. New knowledge is been gained of the virus and possible complications are been seen. Following, we present the case of a 71-year-old man with diagnosis of COVID-19 pneumonia complicated with spontaneous pneumomediastinum.

The harmattan season, which is a period characterized by low temperature, dry air and increased air pollution leads to widespread airborne disease and exacerbation of pre-existing conditions, should be recognized as a period of potential risk of high COVID-19 infection rates. This period also coincides with the Christmas season which comes with so many festivities and can become a COVID-19 super-spreader. With many Nigerians now abandoning the non-pharmaceutical protection measures against COVID-19, the harmattan season and the forthcoming spike in social gatherings might usher in the second wave of the virus which can potentially be more catastrophic. There is need for the Nigerian government to start planning and instituting new protection measures and guidelines for safe Christmas celebration while also educating and encouraging the populace to adopt the protection measures recommended by experts.

Background: In 2004 we started a phase II trial in non-small lung cancer (NSCLC), stage III, with erlotinib followed by a combination with a platinum-based doublet in unselected patients to identify molecular subgroups benefitting from an EGFR targeting approach. Patients and methods: Induction with erlotinib (E, 150 mg, d1-42) was followed by three cycles of gemcitabine (G, 1250 mg/m², d1+d8, q3w) and cisplatin (P, 80 mg/m², d1, q3w). Patients with at least stable disease after E were treated with a GP + E combination. Induction was followed by surgery and radiation. The trial was conducted as a prospective, multi-center, open label, exploratory phase II study to determine pathological response rate (pRR), as well as secondary endpoints disease free survival (DFS) and overall survival (OS). Results: Of 38 prescreened patients 16 were included in the main study. Due to slow recruitment the study had to be terminated early. Combination of E and GP was well tolerated, surgery was feasible after induction therapy in 12 of 16 patients, 7/12 (58%) patients had a major pathological response (MPR). Median overall survival for patients with MPR was 57.7 months (confidence interval (CI), 37.4 to 78.0; n = 7) and for patients without MPR 11.9 months (CI, 6.4 to 17.4; n = 5). 2/16 patients had an epidermal growth factor receptor (EGFR) mutation. Conclusion: Before discovery of distinct molecular mechanisms in NSCLC our study was an attempt to identify clinical and pathological subgroups that would benefit from E induction. Two patients with an EGFR mutation were identified. MPR was a predictor of long term disease free and overall survival.

Introduction: COVID-19 is an infectious disease caused by the severe acute respiratory syndrome coronavirus 2 and it was first reported in China. The aim of this study was to compare clinical features, chest CT findings and laboratory examinations of suspected COVID-19 inpatients according to RT-PCR analysis. Methods: Demographics, comorbidites, symptoms and signs, laboratory results and chest CT findings were compared between positive and negative groups. The study included 292 patients (134 females, 158 males) suspected of COVID-19. All statistical calculations were performed with SPSS 23.0. Results: 158 (54.1%) of the cases were male and 134 (45.9%) were female. Their ages ranged from 17 to 95 years, with an average of 50.46 ± 20.87. A symptom or sign was detected in 86.3% of all patients. The chest CT images of 278 patients were analyzed. Chest CT was negative in 59.2% of patients with positive RT-PCR and 43.9% of patients with negative RT-PCR results. Chest CT findings were atypical or indeterminate in 22.4% of patients with positive RT-PCR results and 20% of patients with negative RT-PCR analysis. ALP, bilirubine, CRP, eosinophil count, glucose, CK-MB mass and lactate were significantly lower in patients with positive RT-PCR test. LDH, lipase, MCV, monocyte, neutrophil count, NLR, platelet, pO2, pro-BNP, procalcitonin, INR, prothrombin time, sodium, troponin T, urea, WBC were significantly lower in patients with positive RT-PCR test results. Conclusion: The diagnosis of COVID-19 is based on history of patient, typical symptoms or clinical findings. Chest CT, RT-PCR and laboratory abnormalities make the diagnosis of disease stronger.

Chronic fatigue syndrome (CFS) is a poorly-understood respiratory condition that affects millions of individuals. Hyperbaric oxygen therapy (HBOT) is a treatment option being considered to address CFS as it is suggested to combat fatigue and increase oxygenation. HBOT provides two opportunities in advancing research of CFS: it may provide data on symptom amelioration and be utilized in the search for a biomarker. By either identifying biomarkers before using HBOT to compare epigenomes of patients before and after treatment or using HBOT to find epigenetic discrepancies between patients with and without treatment, matching epigenetic regulation with symptom amelioration may significantly advance the understanding of the etiology and treatment mechanism for CFS. EPAS1/HIF-2α is a leading candidate for an epigenetic biomarker as it responds differentially to hypoxic and normoxic conditions, which degrades more slowly in hypoxic conditions. Epigenetic regulation of EPAS1/HIF-2α in such differential conditions may be explored in HBOT experiments. In addition to HBOT as a promising treatment option for CFS symptoms, it may aid the identification of biomarkers in CFS. Further research into both outcomes is strongly encouraged.

Meigs syndrome is an uncommon presentation, where a benign ovarian neoplasia presents along with ascites and pleural effusion. About 1% of ovarian neoplasia can present as Meigs syndrome. Patients with Meigs’ syndrome and elevated serum CA-125 are not frequently reported. We report a case of a 50-year-old women who presented with shortness of breath, cough, weight loss of one and half month duration. Chest radiograph of the patient with clinical examination of patient confirms pleural effusion as cause of progressive shortness of breath. The presence of a pelvic mass and elevated serum CA-125, which raised the possibility of malignancy. After complete resection of tumor, the pathologic reports confirmed a benign ovarian neoplasia. We highlight the importance of suspicion, careful general examination, radiological assessment and histological tests to confirm the diagnosis of Meigs’ syndrome.

Introduction: the perennial pandemic: There are serious challenges posed by the SARS-CoV-2 virus and COVID-19 as the disease. With the persistence of the pandemic over one and half year, it is being feared that the COVID-19 may have become the new reality associated with human existence world over and the mankind may have to live with it for years or even decades. Further, the grievous nature of the disease is evolving further with genomic changes in the virus in form of mutations and evolution of variants, with enhanced infectivity and probably virulence. Acute and chronic phases of COVID-19: Epidemiologically, it is becoming clear that apart from the advanced age and pre-existing conditions, such as diabetes, cardiovascular, pulmonary, and renal diseases, certain constituent factors render some patients more vulnerable to more severe forms of the disease. These factors influence the COVID-19 manifestations, its course, and later the convalescence period as well as the newly defined ‘Long COVID phase. The substantial continuing morbidity after resolution of the infection indicates persisting multisystem effects of ‘Long Covid’. Lung damage associated with COVID-19: COVID-19 is primarily a respiratory disease presenting with a broad spectrum of respiratory tract involvement ranging from mild upper airway affliction to progressive life-threatening viral pneumonia and respiratory failure. It affects the respiratory system in various ways across the spectrum of disease severity, depending on age, immune status, and comorbidities. The symptoms may be mild, such as cough, shortness of breath and fevers, to severe and critical disease, including respiratory failure, shock, cytokine crisis, and multi-organ failure. Implications for the post-COVID care: Depending on the severity of respiratory inflammation and damage, as well as associated comorbidities, duration of injury and genetics, the progressive fibrosis leads to constriction and compression of lung tissues and damage to pulmonary microvasculature. Consequently, the COVID-19 patients with moderate/severe symptoms are likely to have a significant degree of long-term reduction in lung function. Depending on the severity of the disease, extensive and long-lasting damage to the lungs can occur, which may persist after resolution of the infection. Managing the long COVID’s challenges: Given global scale of the pandemic, the healthcare needs for patients with sequelae of COVID-19, especially in those with lung affliction are bound to increase in the near future. The challenge can be tackled by harnessing the existing healthcare infrastructure, development of scalable healthcare models and integration across various disciplines with a combination of pharmacological and non-pharmacological modalities. Following clinical and investigational assessment, the therapeutic strategy should depend on the disease manifestations, extent of damage in lungs and other organs, and associated complications.

Cystic fibrosis is explained in this paper that suggests tackling the disease by elimination of the most significant sources of contamination.

Organizing pneumonia (OP), can be seen in association with lung injury, infection, drug intoxication, and connective tissue diseases. Patients of rheumatoid arthritis (RA) are prone to develop interstitial lung disease (ILD), but the pulmonary involvement usually occurs several years after the joint manifestations. Only in about 10% cases of RA, the initial manifestation of the disease can be in the form of interstitial lung disease. OP as the initial manifestation of RA is extremely uncommon occurrence. Here is presented a case of 52-year-old male who presented with OP as the initial manifestation of RA. On investigation, the RA factor and anti-CCP Antibodies were positive. Based on clinical, radiological and histopathological findings the diagnosis was established.

As we know that, Asthma and chronic obstructive pulmonary diseases are well characterized diseases, they can co-exist as asthma-COPD overlap (ACO). The co-existence of asthma-chronic obstructive pulmonary disease overlap (ACO) in chronic obstructive pulmonary disease (COPD) patients is often unrecognized. In patients with a primary diagnosis of COPD or Asthma, the identification of ACO has got implication for better prognosis and treatment. Such patients experience frequent exacerbations, poor quality of life, rapid decline in lung function and high mortality than COPD or Asthma alone. Inhalational steroids provide significant alleviation of symptoms in such patients and some studies suggest that the most severe patients may respond to biological agents indicated for severe asthma. Patients who have asthma with a COPD component tend to present with severe hypoxia because of Irreversible/fixed airway obstruction and impairment of the alveolar diffusion capacity by emphysematous changes. In contrast, patients with COPD who have an asthma component not only have exertional dyspnoea but also develop paroxysmal wheezing or dyspnoea at night or in the early morning. The criteria to diagnose asthma-COPD overlap (ACO) include positive bronchodilator response, sputum eosinophilia or previous diagnosis of asthma, high IgE and/or history of atopy. There is scarcity of literature available in country like India. We highlight the importance of identification of Asthma COPD overlap as different phenotype from COPD or asthma alone as it is challenging to diagnose ACO in India. We report 3 cases having both the features of asthma and COPD, later diagnosed with Asthma-COPD overlap.

Pulmonary mucormycosis is an uncommon pulmonary fungal disease, which is commonly seen in immunocompromised individuals. It is caused by fungi of class Zygomycetes. It constitutes the third most common invasive fungal infection following aspergillosis and candidiasis. Risk factors include patients with hematological malignancies, diabetes mellitus, and immunocompromised states. It is difficult to diagnose early due to non-specific clinical presentation and delay in treatment associated with greater mortality. As we know that Tuberculosis and HIV are highly prevalent in country like India. Post pulmonary tuberculosis is emerging as a risk factor for Pulmonary mucormycosis in the developing countries like India. Patients with non-resolving pneumonia are generally misdiagnosed as Pulmonary tuberculosis. The diagnosis of Pulmonary Mucormycosis is based upon demonstration of fungal hyphae in the clinical specimen. We highlight the importance of clinical suspicion in these cases for early diagnosis and early treatment initiation can reverse morbidity and mortality associated with Pulmonary Mucormycosis. We report 2 cases of Pulmonary mucormycosis present in post-pulmonary tuberculosis patients.

Despite the fact, that lung cancer is more common among older smoking men, however it may also develop among young women without a smoking anamnesis. We report here a history of a non-smoking woman, 40 years old, with a diagnosis of lung adenocarcinoma at IV stage. Despite the fact, the woman received three lines of palliative chemotherapy, the disease progressed. After the sample of the tumor was tested by genetic approach, ROS1 mutation was detected, and the patient was treated with a ROS1 inhibitor, Crizotinib. Sharp improvement was observed already after the first week of treatment. After one-month adenocarcinoma shrink, and specific supraclavicular lymph nodes disappeared. Unfortunately, due to problems with financing the treatment was stopped, after what the disease began to progress rapidly, and the patient died after a month due to brain metastasis. This case is noteworthy also because the patient was first diagnosed a thrombophilia with thrombi present in deep calf veins, left heart ventricle and lungs Adenocarcinoma was discovered occasionally when during video-assisted thoracoscopic surgery biopsy specimen was taken from suspicious mass in the lower lobe of the right lung. This story reminds us that lung carcinoma may start with a paraneoplastic syndrome, like thrombophilia as in this case and finding of adenocarcinoma of the lung in young, non-smoking persons is indicative for possible ROS1 gene mutation. In such cases early treatment with ROS1 protein-tyrosine kinase inhibitors should be started as soon as possible.

This case shown here represents a rare situation where the breast implant is spontaneously and inadvertently migrated from its submammary position via the thoracic wall into the ipsilateral pleural cavity after performing an ipsilateral thoracotomy due to atypical wedge resection of the right upper lobe four months ago. Intraoperatively, the implant has been neither dislodged nor manipulated in any way. In the literature, there are some sparse case descriptions where such breast implant migrations are encountered after VATS procedure (video-assisted thoracoscopy) [2] and open thoracotomy surgery [3]. Interestingly, our case report is quite similar to those which was published by Dutch colleagues in 2014 [4]. Considering the etiology and pathomechanism of such an implant migration as shown here, there is a common agreement that both a leakage of the implant´s fibrous capsule and an operative transection of the intercostal thoracic wall are prerequisite to create a potential migrating pathway to allow implants moving towards the pleural cavity [5]. Additionally, it is believed that the negative pressure within the pleural cavity also alleviates the unidirectional herniation by “sucking in the implant” into the interpleural space [6]. Sometimes, external repetitive pressures such as stretching massages may cause or trigger such an implant dislocation. Furthermore, there are cases described in which, seemingly, implant migration does occur without known preceding thoracic surgery [7]. Eventually, there are cases published in the literature with intrapleural spreading of disrupted breast implant debris [8]. With our patient, thanks to the absence of any discomfort or pain, it was concluded after agreed statement of an interdisciplinary round table discussion not to remove the dislocated implant surgically because of potential intercostal tissue damage and subsequent pain to await. More astonishing, the clinicians involved in this case wondered the fact that the missed implant of her right breast remained either unnoticed or has been completely neglected by the female patient. In this short communication, we present a rare and unusual case of an obviously vanishing breast implant which is found to be inadvertently migrated into the adjacent pleural space after undergoing thoracic surgery. According to common legal policy at our institution, an approval for case reports is generally provided as it was obtained in this particular case.

Pulmonary Alveolar Proteinosis (PAP) is a rare lung disease characterized by excessive accumulation of surfactant lipids and proteins in alveoli and terminal airways. It is caused by impaired GM-CSF signaling [1]. Surfactant is synthesized and secreted by alveolar type II epithelial cells, and removed by uptake and catabolism by these cells, and the alveolar macrophages. Patients with PAP usually describe gradual onset of progressive exertional dyspnea and non-productive cough. However, an asymptomatic presentation is observed in up to 25% of cases, even in the presence of diffuse radiographic changes. Three recognized subtypes exist. Autoimmune PAP is associated with neutralizing GM-CSF autoantibodies and accounts about 90% of cases. Secondary PAP may occur in the context of any disease that reduces the abundance or functionality of alveolar macrophages, resulting in impaired surfactant clearance. Congenital PAP is the result of genetic mutations that disrupt GM-CSF signaling, including mutations in the α- or β-chains of the GM-CSF receptor [1-3].

Introduction - evolution of SARS-CoV-2 variants: With the unrestrained pandemic for over last one-and-half year, SARS-CoV-2 seems to have adapted to its habitat, the human host, through mutations that facilitate its replication and transmission. The G variant incorporating D614G mutation, potently more transmissible than the ancestral virus arose during January 2020 and spread widely. Since then, various SARS-CoV-2 variants of concern (VOCs) and variants of interest (VOIs) with higher infectivity or virulence or both, have evolved on the background of G variant, and spread widely. SARS-CoV-2 infection and the immunodynamics: As the virus becomes more transmissible, its lethality may drop. Apart from the humoral immunity, T-cell recognition from a previous SARS-CoV-2 infection or vaccination may modify the disease transmission correlates and its clinical manifestations. On the other hand, the immunity generated may reduce probability of re-infection as well as limit evolution of adaptive mutations, and emergence of highly infectious and immune-escape variants. There are complex issues related to the SARS-CoV-2 evolutionary dynamics and host’s immunodynamics. Trending etiopathoimmunological correlates: The evolution potential of SARS-CoV-2 is limited because of proofreading function of nsp14. The S protein mutations affect transmissibility, virulence, and vaccine efficacy. The D614G mutation in G variant with higher infectivity has turned the Chinese epidemic into a pandemic. Other SARS-CoV-2 variants, such as Alpha, Beta, Gamma, and Delta seem to have evolved as result of adaptation to selective pressures during periods of prolonged infections and subsequent transmission. Further, there is issue of convergent association of mutations. Basics of immunity and immune system failure: The nature of the immune response after natural SARS-CoV-2 infection is variable and diverse. There are pre-existing neutralizing antibodies and sensitized T cells elicited during previous infection with seasonal CoVs influencing the disease susceptibility and course. The virus has evolved adaptive mechanisms to reduce its exposure to IFN-I and there are issues related to erratic and overactive immune response. The altered neutralizing epitopes in the S protein in SARS-CoV-2 variants modify the immune landscapes and clinical manifestations. Conclusion: current scenarios and prospects: Presently, the SARS-CoV-2 infection is widespread with multiple evolving infectious variants. There is probability of its transition from epidemic to endemic phase in due course manifesting as a mild disease especially in the younger population. Conversely, the pandemic may continue with enhanced disease severity due to evolving variants, expanded infection pool, and changing immunity landscape. There is need to plan for the transition and continued circulation of the virus during the endemic phase or continuing pandemic for indefinite period.