Background Transmission within families and multiple spike protein mutations have been associated with the rapid transmission of SARS-CoV-2. We aimed to: (1) describe full genome characterization of SARS-CoV-2 and correlate the sequences with epidemiological data within family clusters, and (2) conduct phylogenetic analysis of all samples from Yogyakarta and Central Java, Indonesia and other countries. Methods The study involved 17 patients with COVID-19, including two family clusters. We determined the full-genome sequences of SARS-CoV-2 using the Illumina MiSeq next-generation sequencer. Phylogenetic analysis was performed using a dataset of 142 full-genomes of SARS-CoV-2 from different regions. Results Ninety-four SNPs were detected throughout the open reading frame (ORF) of SARS-CoV-2 samples with 58% (54/94) of the nucleic acid changes resulting in amino acid mutations. About 94% (16/17) of the virus samples showed D614G on spike protein and 56% of these (9/16) showed other various amino acid mutations on this protein, including L5F, V83L, V213A, W258R, Q677H, and N811I. The virus samples from family cluster-1 (n = 3) belong to the same clade GH, in which two were collected from deceased patients, and the other from the survived patient. All samples from this family cluster revealed a combination of spike protein mutations of D614G and V213A. Virus samples from family cluster-2 (n = 3) also belonged to the clade GH and showed other spike protein mutations of L5F alongside the D614G mutation. Conclusions Our study is the first comprehensive report associating the full-genome sequences of SARS-CoV-2 with the epidemiological data within family clusters. Phylogenetic analysis revealed that the three viruses from family cluster-1 formed a monophyletic group, whereas viruses from family cluster-2 formed a polyphyletic group indicating there is the possibility of different sources of infection. This study highlights how the same spike protein mutations among members of the same family might show different disease outcomes.
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Background: It has been hypothesized that silent hypoxemia is the cause of the rapid progressive respiratory failure with severe hypoxia that occurs in some patients with COVID-19 without warning. Here, we reported one COVID-19 case with the possibility of silent hypoxemia. Case presentation: A 60-year-old male presented with complaints of cough that he felt starting two weeks before admission without any breathing difficulty. Complaints were accompanied by fever, runny nose and sore throat. Vital signs examination showed blood pressure 130/75 mmHg, pulse 84 times per minute, normal respiratory rate (RR) of 21 times per minute, body temperature 36.5 C, and 99% oxygen saturation with oxygen via nasal cannula 3 liters per minute were recorded. On physical examination, an increase in vesicular sounds and crackles in both lungs were identified. Chest x-ray showed bilateral pneumonia. Nasopharyngeal and oropharyngeal swab real-time polymerase chain reaction tests for COVID-19 were positive. On the third day of treatment, the patient complained of worsening of shortness of breath, but his RR was still normal with 22 times per minute. On the fifth day of treatment, the patient experienced severe shortness of breath with a RR of 38 times per minute. The patient was then intubated and his blood gas analysis showed respiratory alkalosis (pH 7.54, PaO2 58.9 mmHg, PaCO2 31.1 mmHg, HCO3 26.9 mEq/L, SaO2 94.7%). On the eighth day of treatment, his condition deteriorated starting in the morning, with blood pressure 80/40 mmHg with norepinephrine support, pulse 109 times per minute, and 72% SpO2 with ventilator. In the afternoon, the patient experienced cardiac arrest and underwent basic life support, then resumed strained breathing with return of spontaneous circulation. Blood gas analysis showed severe respiratory acidosis (pH 7.07, PaO2 58.1 mmHg, PaCO2 108.9 mmHg, HCO3 32.1 mEq /L, SaO2 78.7%). Three hours later, he suffered cardiac arrest again, but was unable to be resuscitated. The patient eventually died.Conclusions: Silent hypoxemia might be considered as an early clinical sign of deterioration of patients with COVID-19, thus, the physician may be able to intervene early and decrease its morbidity and mortality.
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