In 2003, it was discovered that the entry receptor for the Severe Acute Respiratory Syndrome coronavirus (SARS-CoV) is a protein called the angiotensin-converting enzyme 2 (ACE2). This protein is present in a number of cell types, including those from the respiratory tract. Soon after the emergence of SARS-CoV-2 that is responsible for the disease Covid-19, scientists found that ACE2 was also used by the new coronavirus to infect cells. This opened some interesting possibilities to explain the striking variation in risks of catching and dying from Covid-19. The best recognised of these are the much higher risk of serious illness in older than younger people, in men than women, and in those with pre-existing comorbidities such as hypertension and cardiovascular diseases. There are several ways in which the ACE2 protein might contribute to this variation. The most obvious would be if there is more ACE2, there would be more entry points for the virus to infect the cell, e.g. in older people or in men. However, the evidence for this is rather small, partly because it is not that easy to obtain representative healthy tissues. Alternatively, it could be related to ACE2 membership of a family of proteins that has one end of the protein anchored inside the cell while most of the protein protrudes from the outside of the cell which therefore can be shed when cleaved by proteases at the cell membrane. Herein we review current evidence and theories of ACE2 role on SARS-CoV-2 infectivity and Covid-19 severity.

Aims: The South China Sea (SCS) harbours a rich biodiversity. However, few studies have been published on its diverse communities, particularly its microbial counterparts. As key players behind many of the vital processes carried out in the ocean, microbes are the focus of this study, placing particular emphasis on community composition, structure, and function. Methodology and results: By employing next generation shotgun sequencing technologies (Illumina HiSeq2000), we assessed the taxonomic structure and functional diversity of the prokaryotic communities in surface waters collected from 3 representative sites in the Eastern SCS: Sarawak (Kuching), Sabah (Kota Kinabalu), and Philippines (Manila). Comparisons were undertaken to similar studies from coastal and open ocean environments. All 3 locations were dominated by members of the Proteobacteria (Alpha- and Gamma-) and Cyanobacteria (Synechococcus sp. and Prochlorococcus sp.). The highest proportion of Gammaproteobacteria was found in Sarawak, representing an approximate 20% of total sequences. Archaeal assemblages were made up largely of Euryarchaeota and unclassified sequences, while Crenarchaeota and Thaumarchaeota were present in much smaller proportions, except in the Philippines where Thaumarchaeota made up almost 40% of the entire taxa. Conclusion, significance and impact of study: The majority of the microbial communities adhered to a core set of functional genes across the different locations. However, differences existed particularly in Sarawak waters which are hypothesized to be due to local environmental parameters such as riverine influence. The results obtained from this study provide the first comparison of prokaryotic communities in the surface waters of the eastern SCS and will serve as a good platform for prospective studies in the field of environmental science.

Hypertension is highly prevalent in Malaysia and even the rest of the world. Primary aldosteronism (PA) is one of the most common treatable cause of secondary hypertension. PA occurs due to excessive secretion of aldosterone in the adrenal glands. Up to one in five resistant hypertension cases are due to PA. Therefore, there are a high number of individuals who have the potential to be cured of their hypertension. However, this is difficult to achieve due to limitations in the procedure of diagnosing the PA disease. The challenge now is to know the best usage of available diagnostic methods to detect those who would most likely be cured of hypertension which may be associated with the genotype of the disease. In the past decade, five genes have been found to cause excess aldosterone production in aldosteroneproducing adenomas (APAs), namely KCNJ5, ATP1A1, ATP2B3, CACNA1D and CTNNB1. These somatic mutations have been found to activate the intracellular signaling pathway that regulates aldosterone production. Studies on bilateral adrenal hyperplasia (BAH) samples also have identified the genetic causes for the many hereditary hyperaldosteronism, namely familial hyperaldosteronism types I, II, III, and IV/V. Herein we review the genetic factors of PA as a result of either aldosterone-stimulating somatic mutations or germline variants, and the associated clinical phenotype.