Carl Zimmer Evolution

When we hear the word virus, we usually think of something that makes us sick. A virus is an ultramicroscopic infectious organism that, having no independent metabolic activity, can replicate only within a cell of another host organism. A virus consists of a core of nucleic acid, either RNA or DNA, surrounded by a coating of antigenic protein and sometimes a lipid layer surrounds it as well. The viral genome provides the genetic code for replication, and the host cell provides the necessary energy and raw materials. To fight viruses, we use vaccines. While some may infect a broad range, other viruses can only infect certain kinds of cells. Vaccines are made of inactive, dead or weakened virus cells or protein antigens that can no longer infect

In the article “Are Viruses Alive?,” Luis P. Villarreal discusses the effects of viruses on life, while presenting different angles as to whether or not they are alive themselves and arguing about the impact viruses have had on evolution. Through a deeper understanding of viruses and their functions, the scientific community may come to fully appreciate viruses, whether they are living or non-living in themselves, as significant evolutionary components.

Hilleman’s career life was dedicated to the studying and finding relationships amongst the different diseases causing agents or viruses. As such, the presentation of the finite information about the microorganisms and their associated characteristics opens up the ground for an increased interest in learning how these viruses work to adapt or overcome the body immunity (Offit, 2007). Moreover, through the demonstrations of some of the adaptive features of viruses such as the mutations or change in the gene constitution, Hilleman has illustrated how the process of establishing the specific vaccines for each disease requires comprehensive knowledge and research of the peculiar characteristics of each virus. These elements depicted in Hilleman’s study form the tenets of microbiology and the different disciplines related to subjects such as virology or the study of bacteria. Henceforth, by reading the book, my understanding of the elements of microbiology and the processes of virus control has been emphasized (Offit, 2007). Additionally, the evaluation of the treatment and prevention procedures for some of the common diseases, especially amongst children, has motivated my interest to research and undertake more in operations surrounding vaccinations and control of disease

As stated by Dr. N.A.S, finding a vaccine has been incredibly challenging due to the astonishing genetic diversity of the virus. While it is true that the genome of two HIV infected individuals can differ by up to 30%,6 it is not the integrase enzyme that causes this huge difference in the genomes as written by Dr. N.A.S. Reverse transcriptase is the error prone enzyme that makes multiple mistakes while copying RNA into DNA, which results in ~1 mutation in every new virus.6 The advantage of mutations for HIV is that these new changes are not

“some way must be found to permit the SIV to remain at high levels in people for long enough that such spontaneous mutations might take place. He suggests that the required mechanism is "serial passaging" of virus through unsterile needles. That is, a cut hunter might get an injection while he is still harboring large numbers of viral particles in his bloodstream; that same needle would then be used to infect another person, who might soon receive a second injection, and so forth. High viral population levels can thus be maintained in a series of different people getting shots. With each transfer via contaminated needle, the virus finds itself in a fresh host, with an opportunity to proliferate before the infected person can mount an immune response. Chance mutations can thus accumulate, and eventually the SIV adapts, becoming HIV.”

This, according to the clonal selection theory, the immune system functions on the “ready-made” rather than the “made-to-measure” principle. The question of how an animal makes so many different antibodies there for become a problem of genetics rather than one of protein chemistry” (Bowden 1006). This means that genetics determine how well the immune system works and this the key to figuring out a way to boost the immune system to help fight of infections and diseases before they even begin to weaken and infect the whole body. If someone decided they wanted to be immune to a snake bite or HIV the only thing that would have to be done is find one person just one that is immune and clone that person gene and add it to the other person who also wants to be immune to a certain disease, physical or chemical problem. “Scientist have grown replacement organs for sheep, rats and rabbits using the animal's own cells and alb molds to help the tissue take shape a technique that could be used someday to make spare parts for

There are four main groups of HIV strains (M, N O and P), each with a slightly different genetic make-up. This supports the hunter theory because every time SIV passed from a chimpanzee to a human, it would have developed in a slightly different way within the human body, and produced a slightly different strain. This explains why there is more than one strain of HIV-1 The most studied strain of HIV is HIV-1 Group M, which is the strain that has spread throughout the world and is responsible for the vast majority of HIV infections today. (“origin of HIV & AIDS,”

understood that the pathogens adapted to the immune system and were immune to its defenses so

Where it is still unclear the origins of viruses, one thing is clear, they are a very important part of the horizontal gene transfer, which drastically increases genetic diversity.

Anti-genetic drift is a mechanism for different viruses that involve the accrual of mutations within genes that code for antibody bonding sites.

The most widespread skepticism, however, is based on popular belief that vaccine efficacy is just not satisfactory. Arguing against this, experts explain that IFV is a single stranded RNA (ribonucleic acid) virus with no proofreading mechanism, as is common in their DNA counterparts (Brandenburg et al., 2013). The replication phase of its life cycle is prone to multiple mutations, constantly generating new strains of IFV. Scientist have been frustrated by challenges due to “sequence and antigenic diversity” (Burton et al., 2012), which is analogous to

The main claims of evolution are that all species are connected, species change, and that genes of different species are not identical due to mutations. PBS’s film, What Darwin Never Knew, explains that “all species are connected and they change through Darwin’s ‘descent with modification’ theory” (What Darwin Never Knew). The species are connected, yet varying through mutations. “Mutations are a critical ingredient in the recipe for evolution. Without mutation, everything would stay constant, generation after generation. Mutation generates variation, differences between individuals” (What Darwin Never Knew). In different species, most of the DNA is similar, with the exception of one different sequence. The mutations can cause changes between species, causing variation. Overall, it

IAV is a virus classified as part of the orthomyxoviridae and one of the causative agents of influenza or “the flu”. (Edinger, Pohl & Stertz, 2014) Its natural reservoir is primarily wild aquatic fowl where it is mostly nonpathogenic, though zoonotic infections can occur in mammals and domestic fowl. (Klenk, Matrosovich & Stech, 2008) The jump between species often results in the establishment of highly pathogenic variants that can have devastating effects, as was the case of the “Spanish” influenza pandemic of 1918. (Taubenberger, 2006) The infection across special barriers is dependent on changes to the structure of glycoproteins on the viral envelope, particularly haemagglutinin (HA). The different subtypes of HA and neuraminidase (NA) serve to classify different viral lineages. These changes in the structure can result in proteolytic activation; that when coupled to changes of receptor binding specificity allow for interspecies transmission. (Klenk, Matrosovich & Stech, 2008) The modifications can affect the pathogenicity of the virus even within the same species, which can allow for infection of new cell types, or even systemic disease. (Steinhauer, 1999) These mutations accumulate through successive replications or genetic re-assortment during confection. The resulting structural changes account for the observed antigenic drift that causes loss of immunity despite prior exposures to the virus. This evolutionary process drives the consistent

This is called antigenic "drift." This process allows the virus to make a more stable change yet still evade the immune system. The second type of change is an abrupt change in the hemagglutinin and/or the neuraminidase proteins. This is called antigenic "shift." It isn't as stable of a change but if it does make a successful and complete mutation it can become so deadly that another pandemic. Although Type A viruses undergo both types of changes, Type B only go through the more gradual Type B.

This is not particularly shown with our own biology but with the medicine and that eventually the people who survive the Ebola outbreak will produce offspring that will be most likely be resistant to Ebola. But, the medicine that was given to the people who were affected by Ebola in Kikwit lowered the number of people who would die and who were affected by Ebola. I think that this a piece of evidence that means that humans are forever evolving because this medicine is something that makes us greater and more situated to live on this world. This is not as big of an evolution as the other two examples but it does affect