How do I recover faster from my stomach virus?

Boil ginger and garlic. Take zinc and Vit C supplement. Massage tummy with eucalyptus oil. Nausea means lack of Vitamin B, expecially B6. Chew fresh ginger, take fresh air and rest your stomach from processed foods. Place a warm bottle of water (wrap in cloth) on your tummy. My grandma would burn the rice and make a tea from it, the carbon in it will act as a filter. Do add lemon in your green tea. Make a fresh drink of aloe vera and apple. Rest.vir-sto

Shape of microbes matter in phagocytosis

Phagocytosis is an actin-polymerization-dependent process for the uptake of particles larger than 0.5 μm into cells. Macrophages are cells forming a part of the innate immune system, and phagocytosis is central to their immune function . Phagocytosis is an extraordinarily complex process involving both structural rearrangement (cytoskeletal and membrane) and a complex network of signaling events. Phagocytosis plays a critical role in the clearance of infectious agents or senescent cells and is central to regulating immune responses, inflammation, and tissue remodeling.

Phagocytosis also plays a role in clearing inorganic particulate material from body surfaces such as inhaled carbon or mineral particles. The biochemical mechanisms of phagocytosis have been extensively studied and described in the literature. The phagocytic process essentially involves three steps: recognition by receptors of either an opsonized or nonopsonized particle; receptor-mediated actin polymerization leading to internalization and cleavage of the phagosome from the cytoplasmic surface; and intracellular trafficking for phagosomal maturation. Maturation of the phagosome ultimately leads to the degradation of phagosomal contents and the induction of the appropriate immune responses.

The data shows an increase in the average engulfment time for increased target size, for spherical particles. The uptake time data on nonspherical particles confirms that target shape plays a more dominant role than target size for phagocytosis: Ellipsoids with an eccentricity of 0.954 and much smaller surface areas than spheres were taken up five times more slowly than spherical targets.

Hydrophobic targets are much more susceptible to phagocytosis than the hydrophilic targets (9,18,19). The presence of surface charge (i.e., targets with higher net ζ-potential) also leads to increased uptake: cationic and anionic particles with comparable absolute ζ-potential values have similar levels of ingestion by macrophages (9,14,18–21).

Nonpolar molecules that repel the water molecules are said to be hydrophobic; molecules forming ionic or a hydrogen bond with the water molecule are said to behydrophilic. This property of water was important for the evolution of life.

Water is repelled more by a surface when the hydrophobicity of the surface is increased. The contact angle of a water droplet is larger on a more hydrophobic surface.


Phagocytosis and shape of microbes or other particles

Viruses may be helping deep marine bacteria eat sulfur


“Black smokers”, deep sea vents where hot, sulfur-rich fluids bubble up from beneath the ocean floor, are considered hotspots of microbial activity. They may even be where life originated. Credit: Wikimedia Commons


virus to bac.JPG

Life is no cake walk at the ocean floor, where carbon is scarce and light nonexistent.  At least near deep ocean vents, mineral-rich water bubbles up from magma beneath the crust, providing both heat and a source of energy. In these alien environments, lithotrophs– bacteria that eat minerals instead of organic carbon- have staked out a niche by evolving some creative metabolic strategies.

But minerals are a poor source of energy compared to organic matter. Lithotrophs are slow-growing critters, easily outcompeted when carbon is abundant. They need all the help they can get. And it turns out, they might very well get help… from an unlikely source. A study published last week in Science Express reports how viruses may be helping deep marine bacteria eat sulfur.

Viruses are everywhere- in soils, skies, oceans, plants and animals, even deep beneath the ocean floor.  In spite of their ubiquity, it’s not well-known how viruses influence marine bacteria and the nutrient cycles they drive.

To study the impact of viruses on sulfur-eating bacteria, a team of scientists led by Dr. Karthik Anatharaman at the University of Michigan collected samples from five different hydrothermal vents : four in the Western Pacific Ocean and one in the Gulf of California. They used shotgun metagenomic sequencing to look at the genomes of the bacteria and viruses present in these environments.

The researchers found five different virus “types” that carried two genes involved in sulfur metabolism. Known as rdsrA and  rdsrC, these genes encode different pieces of dissimilatory sulfite reductase, an enzyme that breaks down elemental sulfur.

How and why did viruses come to acquire these genes? Not technically considered alive, viruses don’t really need enzymes because they don’t perform metabolism on their own. A virus’s sole purpose is to infect a host with its genetic code so that it can turn the host cell into a virus factory. But during viral replication, pieces of  DNA can be accidentally snipped out of the host and integrated into the viral genome. The scientists found bacteria in the same samples carrying both the rdsrAand rdsrC genes. It’s likely that accidental incorporation of host DNA is how viruses ended up with sulfur genes in the first place.

While acquiring sulfur genes may have been a complete accident, viruses appear to have been actively maintaining those genes for a long time.

When the scientists compared rdsrA and rdsrC from viral and bacterial genomes, they found something interesting: completely different DNA sequences surrounding the genes. If viruses had acquired sulfur genes during recent replication errors, some of the nearby DNA would probably have come along for the ride as well. That completely different DNA sequences surround the sulfur metabolism genes in bacteria and viruses suggests viruses have been passing along rdsrgenes, generation to generation, for a very long time. In other words, sulfur metabolism genes are beingmaintained  in viruses by natural selection.

Why would deep sea viruses bother to maintain sulfur metabolism genes they don’t use?  It turns out these viruses may actually have a use for sulfur genes, albeit an indirect one: helping out their hosts. By carrying genes that bacteria can make use of, viruses may assist their hosts in acquiring energy. The ability of sulfur-eating bacteria to acquire energy is ultimately limited by how quickly they can decode their sulfur genes to build enzymes that can do the work. But if a bacteria were to contain viruses with extra copies of the genes it needs, that could help speed the process along. In essence, when a sulfur virus infects a sulfur bacteria, it donates genes that its host can use.

What’s a virus to gain from all of this? Remember, a virus’s sole purpose is replication. Staying in your host’s good graces has its perks. An “infected” bacteria that can acquire energy faster than its neighbors may be able to grow and reproduce faster- leading to more infected offspring, and more viruses. By supplementing host metabolism, viruses may help ensure their continued survival.

This study sheds light on a potentially widespread, mutually beneficial ecological interaction between bacteria and viruses. Lithotrophs in the deep ocean play an important role in the global sulfur cycle and have done so for billions of years. By giving an adaptive advantage to sulfur-eaters and helping them survive, it’s possible viruses have played an equally important role in the geochemical evolution of our planet.

Credit: Wikimedia Commons

Imagine you were forced to live in perpetually subzero temperatures, with no oxygen, no light, and way more salt than your system could handle. How would you manage? One way might be to get extremely small. At least, that seems to be what’s happening in a frozen Antarctic lake that’s cut off from the rest of the world by 27 meters of perennial ice.

lake vida.JPG

Lake Vida, Antarctica, has come under biological scrutiny recently. It’s an fascinating environment for a number of reasons. For one, it represents a unique combination of extreme conditions. Vida’s high salt concentrations keep the lake’s water liquid at -13.4ºC, or 7.9 ºF. And, even more intriguing, this super-chilled salt bath has been cut off from the outside world for nearly 3,000 years.

The microbial inhabitants of Lake Vida have had a unique opportunity to evolve in complete isolation. For microbial ecologists, this means a potential goldmine of novel adaptations and genetically unique organisms.

Approximate location of Lake Vida, Antarctica. Credit: Wikimedia Commons

So far, Lake Vida’s microbes have lived up to expectations. In a study published recently in the journalApplied and Environmental Microbiology, Dr. Alison Murrary and colleagues find Lake Vida’s brine is teeming with some very tiny critters. These ultrasmall microbes, or ultramicrocells, are roughly 200 nanometers in diameter, just undercutting the theoretical “lower size limit” for a single-celled organism. In addition, these tiny critters display some fascinating adaptations for handling the stress of life in cold, salty brine.

Murray and colleagues used several techniques to characterize the ecology of Lake Vida brine samples collected in 2010, including scanning electron microscopy, spectroscopy, and x-ray diffraction.

In their recent study, the scientists observed two cell populations in Lake Vida’s brine. One population of rod-shaped bacteria ranged in size from ~0.4-1.5 µm, while a smaller class of spherical bacteria were approximately ~0.2 µm, or 200 nanometers, in diameter. This second class, designated the “ultrasmalls”, was 100 times more abundant than their larger counterparts. Even smaller particles that ranged in size from 20-140 nanometers were also abundant.

Further analysis using x-ray spectroscopy indicated that both ultrasmalls and nanoparticles had granular, iron-rich surface coatings. Interestingly, these coatings resemble iron oxide minerals found in old, weathered soils. It was also common for ultrasmalls to possess exopolysaccharides– long, filamentous proteins- connecting them to the nanoparticles.

Exopolysaccharides can serve many functions for microorganisms. In this case, the scientists speculate exopolysaccharides act as a nucleation site for iron particles- that is, a surface to which iron particles can precipitate in solid form. The resultant “iron exoskeleton” may be a unique adaptation for protection against extreme cold.

The nanoparticles remain something of a mystery, but the scientists hypothesize these may also be a part of an elaborate ultrasmall survival strategy. The size and morphology of the nanoparticles suggests they may, in fact, be extracellular membrane vesicles– pieces of cells that have popped off their parent and become self-contained storage units . Other scientists have found that microbes produce such vesicles in response to temperature stress. Like a storage unit, vesicles allow microbes to sweep their house clean, removing unnecessary clutter. One sort of unwanted baggage for the Lake Vida ultrasmalls may be misfolded proteins. Protein misfolding is a common problem in subzero environments. Harboring useless misfolded proteins represents a drain on valuable cellular resources.


Europa, Jupiter’s icy moon, has excited astrobiologists as a potential site for extraterrestrial life in our solar system. Credit: Wikimedia Commons

Lots of open questions remain regarding the ecology of Lake Vida’s ultrasmalls. Perhaps the biggest question iswhy exactly these microbes are so tiny. There are a number of possibilities to be explored. Smallness is a response to stressful environments across all domains of life. Hyperosmotic stressthe result of being bathed in a super salty liquid- may result in water loss and cell shrinkage. Or ultrasmalls may be expending so much energy dealing with the cold that they don’t have the extra resources required to grow bigger.

Answering these questions will help scientists understand how microbes may cope with extreme environments not only on Earth, but on icy extraterrestrial worlds as well.


Viruses are the most abundant biological entities in the oceans and a pervasive cause of mortality of microorganisms that drive biogeochemical cycles. Although the ecological and evolutionary effects of viruses on marine phototrophs are well recognized, little is known about their impact on ubiquitous marine lithotrophs. Here, we report 18 genome sequences of double-stranded DNA viruses that putatively infect widespread sulfur-oxidizing bacteria. Fifteen of these viral genomes contain auxiliary metabolic genes for the α and γ subunits of reverse dissimilatory sulfite reductase (rdsr). This enzyme oxidizes elemental sulfur, which is abundant in the hydrothermal plumes studied here. Our findings implicate viruses as a key agent in the sulfur cycle and as a reservoir of genetic diversity for bacterial enzymes that underpin chemosynthesis in the deep oceans.

Copyright © 2014, American Association for the Advancement of Science.

Inhalation of ozone and sulfur dioxide inhibited influenza virus growth in the nose of mice. Ozone inhalation caused the more pronounced inhibition of influenza virus growth: 0.6 ppm ozone for 3 hours post-virus exposure almost completely inhibited influenza virus growth in the nose, whereas sulfur dioxide (6 ppm for 7 days) causes only partial inhibition of influenza growth in the nose. Neither gas altered the propagation of influenza virus in the lungs of mice. Vesicular stomatitis virus (VSV) growth was either unaffected by exposure to ozone (0.9 ppm for 3 hours) or, when ozone exposure preceeded VSV exposure, the virus may have grown to slightly higher titer. The inhibitory effect of ozone and sulfur dioxide on influenza virus growth in nasal epithelium suggests a competitive interaction between the chemical inhalant, the virus, and host tissues, with net consequences for the pathogenesis of this disease. If the effcts of these inhalants are to be properly interpreted, they should be determined for all major regions of virus growth and inhalant deposition.