To halt the pandemic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), governments around the world have imposed policies, such as lockdowns, mandatory mask wearing, and social distancing. The application of disinfecting materials in shared public facilities can be an additional measure to control the spread of the virus. Copper is a prominent material with antibacterial and antiviral effects. In this study, we synthesized copper nanoparticles (CuNPs) as a surface coating agent and assessed their antiviral activity against SARS-CoV-2. CuNPs with a mean size of 254 nm in diameter were synthesized from copper sulfate as a source and were predominantly composed of copper oxide. The synthesized CuNPs were mixed with resin-based paint (CuNP/paint) and sprayed on the surface of stainless steel remnants. SARS-CoV-2 lost 97.8% infectivity on the CuNP/paint-coated surface after 30 min of exposure and more than 99.995% infectivity after 1 h of exposure. The inactivation rate was approximately 36-fold faster than that on the paint alone-coated and uncoated surfaces. The CuNP/paint-coated surface showed powerful inactivation of SARS-CoV-2 infectivity, although further study is needed to elucidate the inactivation mechanisms. Applications of CuNP/paint coatings to public or hospital facilities and other commonly touched areas are expected to be beneficial.
We isolated an avian influenza A/H9N2 virus from an apparently healthy chicken at a live-poultry market in January 2018. This is the first report of a whole-genome sequence of A/H9N2 virus in Indonesia.
A total of 120 cloacal swab samples were collected from asymptomatic-ducks traded at a live-bird market in East Java-Indonesia during January to February 2017. After virus isolation using 10-days-old embryonated chicken eggs, hemagglutination activity was tested. TaqMan real-time reverse transcription (RT) polymerase chain reaction (PCR) assay was performed employing primer sets to differentiate HA genes of H5 clade 2.1.3 and clade 2.3.2
.1. Our result show that Avian influenza virus (AIV)-A/H5 clade 2.3.2.1 was currently prevalent among ducks in a live-poultry market (LPM), indicating LPM could be an important place as an entry point of avian viruses to human resulting novel reassortant strain.
Background
Influenza A viruses are a major pathogen that causes significant clinical and economic harm to many animals. In Indonesia, the highly pathogenic avian influenza (HPAI) H5N1 virus has been endemic in poultry since 2003 and has caused sporadic deadly infections in humans. The genetic bases that determine host range have not yet been fully elucidated. We analyzed the whole-genome sequence of a recent H5 isolate to reveal the evolution toward its mammalian adaptation.
Methods
We determined the whole-genome sequence of A/chicken/East Java/Av1955/2022 (hereafter, “Av1955”) from a healthy chicken in April 2022 and conducted phylogenetic and mutational analysis.
Results
Phylogenetic analysis revealed that Av1955 belonged to the H5N1 clade 2.3.2.1c (Eurasian lineage). The six gene segments (PB1, PB2, HA, NP, NA, and NS) out of the eight segments derived from viruses of H5N1 Eurasian lineage, one (PB2) from the H3N6 subtype and the remaining one (M) from the H5N1 clade 2.1.3.2b (Indonesian lineage). The donor of the PB2 segment was a reassortant among three viruses of H5N1 Eurasian and Indonesian lineages and the H3N6 subtype. The HA amino acid sequence contained multiple basic amino acids at the cleavage site. Mutation analysis revealed that Av1955 possessed the maximal number of mammalian adaptation marker mutations.
Conclusions
Av1955 was a virus of H5N1 Eurasian lineage. The HA protein contains an HPAI H5N1-type cleavage site sequence, while the virus was isolated from a healthy chicken suggesting its low pathogenicity nature. The virus has increased mammalian adaptation markers by mutation and intra- and inter-subtype reassortment, gathering gene segments possessing the most abundant maker mutations among previously circulating viruses. The increasing mammalian adaptation mutation in avian hosts suggests that they might be adaptive to infection in mammalian and avian hosts. It highlights the importance of genomic surveillance and adequate control measures for H5N1 infection in live poultry markets.
In Indonesia, highly pathogenic avian influenza A/H5N1 virus has become endemic and was linked to direct transmission to humans. During 2013 to 2014, we isolated avian influenza A/H5N1 and A/H3N6 viruses from poultry in Indonesia. This study aimed to reveal their pathogenicity in mammals using a mouse model. Three of the isolates, Av154 of A/H5N1 clade 2.3.2.1c, Av240 of A/H5N1 clade 2.1.3.2b, and Av39 of A/H3N6, were inoculated into BALB/c mice. To assess morbidity and mortality, we measured body weight daily and monitored survival for 20 days. Av154-and Av240-infected mice lost 25% of the starting body weight by day 7, while Av39-infected mice did not. Most of Av154-infected mice died on day 8, while majority of Av240-infected mice survived until day 20. A 50%mouse lethal dose was calculated to be 2.0x10 1 50%-egg infectious doses for Av154, 1.1x10 5 for Av240, and >3.2x10 6 for Av39. Av154 virus was highly virulent and lethal in mice without prior adaptation, suggesting its high pathogenic potential in mammals. Av240 virus was highly virulent but modestly lethal, and Av39 virus was neither virulent nor lethal. Several mammalian adaptive markers of amino acid residues were associated with the highly virulent and lethal phenotypes of Av154 virus. 1) Av154: A/turkey/East Java/Av154/2013(H5N1) clade 2.3.2.1.c Eurasian lineage 2) Av240: A/chicken/East Java/Av240/2014(H5N1) clade 2.1.3.2b Indonesian lineage 3) Av39: A/duck/East Java/Av39/2013(H3N6). 4) Mammalian adaptive amino acid residue is highlighted by bold and light blue of background color.
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