Lifeboat Foundation

Scientists around the world are tracking at least eight strains of coronavirus around the world, using genetic detective work to show how the virus spreads.

Researchers say the virus appears to mutate very slowly, with only tiny differences between the different strains, and that none of the strains of the virus is more deadly than another.

Continue reading “Map shows how eight strains of coronavirus raced around the world” »

An interesting opinion:

The US Government Comparative Toxicogenomics database shows that Fluoride can inhibit Human immunity to viruses and pneumonia. Angiotensin I-Converting Enzyme (ACE), 2’-5’-Oligoadenylate Synthetase 1 (OAS1) and Intercellular Adhesion Molecule 1 (ICAM1) are included as susceptible epigenetic targets of the poison.

Read 3 answers by scientists with 1 recommendation from their colleagues to the question asked by Geoff Pain on Feb 4, 2020.

Continue reading “Could areas of high Fluoride ingestion be more susceptible to Coronavirus outbreaks?” »

There are endless viruses in our midst, made either of RNA or DNA viruses, which exist in much greater abundance around the planet, are capable of causing systemic diseases that are endemic, latent, and persistent—like the herpes viruses (which includes chicken pox), hepatitis B, and the papilloma viruses that cause cancer. “DNA viruses are the ones that live with us and stay with us,” Denison said. “They’re lifelong.” Retroviruses, like H.I.V., have RNA in their genomes but behave like DNA viruses in the host. RNA viruses, on the other hand, have simpler structures and mutate rapidly. “Viruses mutate quickly, and they can retain advantageous traits,” Epstein told me. “A virus that’s more promiscuous, more generalist, that can inhabit and propagate in lots of other hosts ultimately has a better chance of surviving.” They also tend to cause epidemics—such as measles, Ebola, Zika, and a raft of respiratory infections, including influenza and coronaviruses. Paul Turner, a Rachel Carson professor of ecology and evolutionary biology at Yale University, told me, “They’re the ones that surprise us the most and do the most damage.”

Scientists discovered the coronavirus family in the nineteen-fifties, while peering through early electron microscopes at samples taken from chickens suffering from infectious bronchitis. The coronavirus’s RNA, its genetic code, is swathed in three different kinds of proteins, one of which decorates the virus’s surface with mushroom-like spikes, giving the virus the eponymous appearance of a crown. Scientists found other coronaviruses that caused disease in pigs and cows, and then, in the mid-nineteen-sixties, two more that caused a common cold in people. (Later, widespread screening identified two more human coronaviruses, responsible for colds.) These four common-cold viruses might have come, long ago, from animals, but they are now entirely human viruses, responsible for fifteen to thirty per cent of the seasonal colds in a given year. We are their natural reservoir, just as bats are the natural reservoir for hundreds of other coronaviruses. But, since they did not seem to cause severe disease, they were mostly ignored. In 2003, a conference for nidovirales (the taxonomic order under which coronaviruses fall) was nearly cancelled, due to lack of interest. Then SARS emerged, leaping from bats to civets to people. The conference sold out.

SARS is closely related to the new virus we currently face. Whereas common-cold coronaviruses tend to infect only the upper respiratory tract (mainly the nose and throat), making them highly contagious, SARS primarily infects the lower respiratory system (the lungs), and therefore causes a much more lethal disease, with a fatality rate of approximately ten per cent. (MERS, which emerged in Saudi Arabia, in 2012, and was transmitted from bats to camels to people, also caused severe disease in the lower respiratory system, with a thirty-seven per cent fatality rate.) SARS-CoV-2 behaves like a monstrous mutant hybrid of all the human coronaviruses that came before it. It can infect and replicate throughout our airways. “That’s why it is so bad,” Stanley Perlman, a professor of microbiology and immunology who has been studying coronaviruses for more than three decades, told me. “It has the lower-respiratory severity of SARS and MERS coronaviruses, and the transmissibility of cold coronaviruses.”

For the first time, scientists have reprogrammed cells from a 114-year-old woman into induced pluripotent stem cells (iPS cells), a move which they describe as a significant step toward understanding “the underlying mechanisms of extreme longevity and disease resistance.”

iPS cells are adult cells that have been genetically reprogrammed into an embryonic stem cell-like state and are able to give rise to any of the specialized cell types of the body, whether it’s neurons, blood cells, or heart cells.

Until this new project, researchers weren’t even certain whether they could create viable iPS cells from someone so elderly, let alone a supercentenarian. Now they have shown it’s possible to effectively make these aged cells resemble young pluripotent cells, the researchers believe they might have made a step towards the reversal of cellular aging.

Circa 2017

Plant viruses, the simple obligate intracellular parasites with small genomes, rely entirely on host machineries for their life cycle including replication, intracellular (cell-to-cell) and systemic movement (Nelson and Citovsky, 2005). Virus infections pose serious threats to agriculture and cause huge economic losses. Despite encoding only a limited number of proteins, numerous interactions of viral RNAs/proteins with host factors have puzzled the plant virologists for over a century and the complexity of these interactions is just becoming understood.

Plants have developed two major strategies to counteract virus infections: resistance (R) gene-mediated, and RNA silencing-based defenses. In addition, the mutation in essential genes for viral infection also causes plant resistance against viruses, called recessive gene-mediated resistance. These approaches have been used in crop protections and have shown significant economic impact (Abel et al., 1986; Whitham et al., 1996; Baulcombe, 2004; Kang et al., 2005; Wang and Krishnaswamy, 2012).

This Research Topic combines 13 publications, including 9 review articles and 4 research articles, covering almost every aspect of plant-virus interactions. The featured in-depth topic reviews in various sub-fields provide readers a convenient way to understand the current status of the related sub-fields and the featured research articles expand the current knowledge in related sub-fields.

Most simply, the phrase “genome editing” represents tools and techniques that biotechnologists use to edit the genome — that is, the DNA or RNA of plants, animals, and bacteria. Though the earliest versions of genome editing technology have existed for decades, the introduction of CRISPR in 2013 “brought major improvements to the speed, cost, accuracy, and efficiency of genome editing.”

CRISPR, or Clustered Regularly Interspersed Short Palindromic Repeats, is actually an ancient mechanism used by bacteria to remove viruses from their DNA. In the lab, researchers have discovered they can replicate this process by creating a synthetic RNA strand that matches a target DNA sequence in an organism’s genome. The RNA strand, known as a “guide RNA,” is attached to an enzyme that can cut DNA. After the guide RNA locates the targeted DNA sequence, the enzyme cuts the genome at this location. DNA can then be removed, and new DNA can be added. CRISPR has quickly become a powerful tool for editing genomes, with research taking place in a broad range of plants and animals, including humans.

A significant percentage of genome editing research focuses on eliminating genetic diseases. However, with tools like CRISPR, it also becomes possible to alter a pathogen’s DNA to make it more virulent and more contagious. Other potential uses include the creation of “‘killer mosquitos,’ plagues that wipe out staple crops, or even a virus that snips at people’s DNA.”

A large team of researchers affiliated with multiple institutions in and around Hangzhou, China, has taken a very large step toward the creation of a comprehensive human single-cell atlas. In their paper published in the journal Nature, the group describes how they sequenced the RNA of over a half-million single cells donated by volunteers and processed the information to present it in a way that could be used in a single-cell atlas.

All of the cells in the human body carry the same basic genetic information—they differ in which genes are expressed. Those genes that are expressed define the function of a given cell. For some time, medical researchers have wanted an atlas that would describe which genes are expressed in cells in all parts of the body. Such an atlas would help scientists better understand the functions of cells and how they work together, in addition to saving time on new research efforts. Atlases have been created for some tissue types, but currently, there is no single atlas to cover all of the cell types in the human body. Creating such an atlas would require much time and effort over many years, as the human body has over 30 trillion cells, after all. In this new effort, the researchers have taken a large step toward that goal by providing gene expression information for over 500,000 cells from different parts of the body (and some from fetal tissue), including all of the major organs.

The work involved first obtaining the tissue samples and then processing them. To that end, the cells were first isolated by putting some in a centrifuge and using enzymes with others. Once isolated, each of the cells were sequenced using a special tool the team previously developed called Microwell-seq—it allows for fast sequencing of large numbers of cells. In all, the team sequenced cells from 60 types of tissue. The researchers then generated a map using a method they devised for classifying cell information. The map and its underlying data form the basis of what could become a full, comprehensive single-cell database.

:33333 could lead to future cures of muscular dystrophy.

Facioscapulohumeral muscular dystrophy (FSHD) is caused by altered expression of DUX4, a gene important during development that is not usually present in adult cells. In FSHD skeletal muscle, activation of DUX4 leads to apoptosis. To identify potential targets that mediate DUX4-induced cell death, Lek et al. performed an unbiased screen using CRISPR-Cas9. Hypoxia signaling emerged as a target, and treating patient cells and zebrafish models of FSHD with inhibitors of hypoxia signaling reduced cell death and expression of DUX4 target genes and improved structural defects and muscle function. Results demonstrate the utility of this CRISPR-Cas9 screen for identifying putative therapeutic targets for FSHD.

The emergence of CRISPR-Cas9 gene-editing technologies and genome-wide CRISPR-Cas9 libraries enables efficient unbiased genetic screening that can accelerate the process of therapeutic discovery for genetic disorders. Here, we demonstrate the utility of a genome-wide CRISPR-Cas9 loss-of-function library to identify therapeutic targets for facioscapulohumeral muscular dystrophy (FSHD), a genetically complex type of muscular dystrophy for which there is currently no treatment. In FSHD, both genetic and epigenetic changes lead to misexpression of DUX4, the FSHD causal gene that encodes the highly cytotoxic DUX4 protein. We performed a genome-wide CRISPR-Cas9 screen to identify genes whose loss-of-function conferred survival when DUX4 was expressed in muscle cells. Genes emerging from our screen illuminated a pathogenic link to the cellular hypoxia response, which was revealed to be the main driver of DUX4-induced cell death.

Scientists took conspiracy theories seriously and analyzed the coronavirus to reveal its natural origins.