مُلاّ جان محمد
افسوس ہے گذشتہ مہینہ ہمارے دومخلص قومی کارکن ملاجان محمدکلکتہ اورمولانا محمد عاقل الٰہ آباد انتقال کرگئے۔ملا صاحب کااصل وطن پشاور تھالیکن عرصہ دراز سے کلکتہ میں آبسے تھے اوراب سچ مچ وہی ان کاوطن تھا۔نہایت پُرجوش،جری اوربیباک انسان تھے۔گذشتہ نصف صدی میں کوئی قومی اور ملی تحریک ایسی نہیں ہے جس میں انہوں نے بڑھ چڑھ کراورولولہ و عزم کے ساتھ حصہ نہ لیا ہو۔ ان کی علمی زندگی کاآغاز تحریک خلافت سے ہوا اوراختتام مجلس مشاورت پر۔کلکتہ میں شاید ہی کوئی مسلم ادارہ(یہاں تک کہ محمڈن اسپورٹنگ کلب بھی) ایسا ہوجس میں ملاصاحب نے نمایاں حصہ نہ لیاہو۔اسی وجہ سے وہ کلکتہ کے لوگوں میں بے حد مقبول تھے۔ بڑے بے غرض،بے لوث اورنہایت سادہ اورمخلص مسلمان تھے۔۱۹۵۰ء میں کلکتہ کے فساد میں لوگوں نے ان کو بچوں کی طرح چیختے اور روتے دیکھا ہے۔ عمر۸۵ سال کے قریب تھی۔ [نومبر ۱۹۷۲]
The novel Corona Virus (nCoV-2019), clouded the entire world during the year 2020; with its emergence in December 2019 from Wuhan, China. The nCoV-19 is a novel variant of the Coronavirus family, with its predecessors been implicated for the pandemics of Middle East Respiratory Syndrome (MERS-CoV) and Severe Acute Respiratory Syndrome (SARS-CoV); that caused flu-like condition and respiratory distress symptoms [1-6]. The viral strain also intrudes on extra-pulmonary relevance; being involved with deranging immunity as evidenced by lymphopenia and a prolonged prothrombin time; it impacts cardiomyocytes and pancreatic tissue directly [7-11]. These implications of nCoV-19 does suggest a long-term relevance of the disease profile. The emergenceof nCoV-2019 was quick to gain a pandemic status worldwide. An immense shift in the influx of the type of patients was observed, that imparted a false impression of a reduction in cardiovascular and metabolic patient presentation; formerly that had been the majority engaging the worlds’ healthcare facility. But as the world prepares itself for a possible second wave of the n-CoV-19, a prudent approach would be to remind us of the history lessons from the previous corona-led pandemic, such as MERS and SARS. This editorial will emphasize on channeling our focus to nCoV-19 implications on cardiovascular and metabolic disorders. The pandemics of SARS-CoV during 2002-2003 and MERS-CoV in 2012 highlight the long term relevance of coronavirus to cardiac and metabolic disease pathologies, both during and in the aftermath of these pandemics [3]. The SARS-CoV had demonstrated an increase of cardiovascular problems by 44%, hyperlipidemia by 68% and diabetes mellitus by 60%, in people who had recovered from the viral attack [12, 13]. Likewise, MERS-CoV had also embarked an increase of cardiac disorders by 30% and hypertension by 50% and diabetes mellitus by 50% [3, 8, 9]. Published research on nCoV-19 has hinted for a similar rising trend of cardiovascular and metabolic complexities. An increase in cardiac troponin level is observed with increased cases of myocarditis and heart failure [14]. A 20% increase in the incidence of diabetes and a 40 % rise in cardiovascular and cerebrovascular diseases is observed with nCoV-19 [8, 9]. Little do we comprehend that the involvement of angiotensin converting enzyme 2 (ACE2) receptors could play havoc on endothelium, kidney, intestine, liver and any other organ [15]. The nCoV-19 has thrown a curveball to the realm of the worldwide health and financial setting. Even with the current economic predicament it does seems prudent to be prepared in advance for the long term consequences of this pandemic. The bigger question would be to, not just direct our efforts at countering the possible second wave of nCoV-19 but also for the possible chaos of cardiovascular and metabolic disease outfall, impacting the world health system.
Hepatitis is a fatal disease of the liver caused by the Hepatitis Viruses including Hepatitis C Virus (HCV). HCV has an RNA genome and it frequently changes its genetic makeup giving rise to variants. The rate of change in the viral genome is higher in cases where the infection is uncontrolled, and the virus gets more chances to replicate. With > 6% of the general population infected with HCV, the burden of HCV infection is increasing in Pakistan mostly attributed to failure of control strategies. Response rate of anti-viral drugs used for the treatment of chronic Hepatitis C infection in different geographical regions reflect the diversity of the virus as well as the response of particular ethnic groups. Characterization of seven genetic lineages (genotypes 1-7) among the susceptible and resistant HCV types, in combination with other markers possibly will help manage HCV infected patients with respect to selection of appropriate antiviral therapy and future vaccine development against the virus. In the present study the existing pattern of HCV genotypes distribution was investigated in Peshawar, Khyber Pakhtunkhwa Province of Pakistan and characterization of HCV genotype 3a was carried out based on sequencing and phylogenetic analysis of HCV Core and non-structural protein NS5B for detection of clinically relevant mutations which may be related with response to conventional Interferon and Ribavirin combination therapy. In total 422/510 (82.75%) PCR positive samples examined by a modified type-specific PCR based assay and sequencing of the Core gene, 45.5% were identified as having HCV 3a infection. Mixed genotypic infection was detected in 22.99% of patients. Genotype 1b accounted for 11.61% while 3b was present in 5.21% of patients. Rare genotypes encountered were 2a (4.98%), 2b (3.79%) and 1a (3.32%) respectively. Patients with confirmed status of genotype 3a infection were evaluated for variables of interest at various intervals of therapy. Among 100 patients who completed therapy for 24 weeks, 43% of the patients achieved Sustained Virological Response (SVR), while 57% of the patients turned out to be Non-Responders (NRs). Mean age of the patients was low (34 ± 9.8) among patients who achieved SVR than those with non-response. The 24 weeks ALT levels were significantly low among patients with SVR as compared to NRs (p-value ≤ 0.05). The association of Early Virological Response (EVR) with SVR was found statistically significant (p-value ≤ 0.05). HCV NS5B (polymerase gene) and Core gene were sequenced in patients with SVR and NRs. Sequence comparison of amino acids in the pre and post-therapy isolates against HCV 3a reference sequence (Isolate NZL1; BAA04609), revealed that the Core region of HCV was highly conserved among all the isolates with no obvious variations between SVR and NR sequences. Full length NS5B sequence revealed four novel mutations (A67V, T131I, R374H and M425L) significantly associated with SVR (p-value ≤ 0.05) in Pakistani HCV 3a isolates. Phylogenetic analysis of the obtained viral genomic sequences based on HCV 3a Core and NS5B gene sequences with reference sequences from different countries showed that different strains of HCV genotype 3a are prevalent in Peshawar. Conclusion The present study reports that the pattern of HCV subtypes distribution in Peshawar, KP province has changed over times. Although less than previously reported; HCV 3a, still accounts for most of the HCV infections in Peshawar. There is increasing burden of HCV 1b or mixed infections of 1b with other types which may have consequences for disease management strategies. Phylogenetic analysis on the basis of HCV 3a Core and NS5B gene sequences indicated the presence of different lineages of HCV genotype 3a in Peshawar. Moreover, the study reveals that EVR and viral genetic mutations in NS5B region of HCV 3a can help predict treatment response among the chronically infected HCV 3a patients in Peshawar.