H1N1 Influenza Virus: The Evolutionary Analysis Of

There are various genetic changes that people can experience the ill effects of that will presumably never be finished unless we effectively mediate and genetic engineering the cutting edge to withstand these issues. Case in point, Cystic Fibrosis, a dynamic and risky sickness for which there is no known cure, could be totally cured and annihilated with the assistance of particular genetic engineering, so it can almost never aging effect humans.

Every year, millions of people start talking about the influenza virus and getting their vaccines as the flu season approaches, which starts around the October-November period and reaches its peak between December and March. Therefore, public health officials around the world- and in the U.S in particular- are constantly challenged by properly preparing for the annual influenza dilemma, given that this viruses, and other respiratory viruses, are a serious health threat to the U.S population and the world as a whole. Furthermore, what makes the influenza virus even more challenging to control is that it can mutate rapidly and reassort to form new strains, having the ability to reside in multiple animal hosts. In fact, many scientists and researchers have been doing in-depth intensive research so as to understand the mechanism behind this unique characteristic of the virus, try to find new ways to control it, and explore different areas of protection and vaccination.

Willcox et al. investigate a group of elderly males that could potentially influence factors in healthy human ageing by studying potential longevity candidate genes linked to the insulin/IGF-1 signalling (IIS) pathway. The Authors state that previous research indicates that the only human gene found to be widely associated with the effects of longevity and healthy ageing is the ApoE gene. The Authors performed a study on a group of genes that were chosen for their relation to ageing phenotypes sourced from previous model organisms. The

It is a known fact that all measures of physiological function decline in human aging. While genetics certainly play a role in the declining of physiological function with age, it can be argued that a fundamental part of aging can be reflected by chemical processes resulting in the appearance of harmful side products of the normal metabolism over time. When enzymes speed up reactions it is harder to slow them down. At the same time side reactions are constantly occurring and more and more unwanted side products are continuously being formed.

Influenza virus has caused serious respiratory illness and death over the past centuries. Epidemics and pandemics due to Influenza virus were known to cause morbidity and mortality in humans and other animals. Pandemics have been documented since the 16th century (WHO, 2005) and in the last 400 years, at least 31 pandemics have been recorded (Lazzari and Stohr, 2004). Influenza virus belongs to the family Orthomyxoviridae, which is characterized by a segmented, minus-stranded RNA genome. Influenza viruses are irregular, spherical (80-120 nm diameter) or filamentous structures and their surfaces are studded with rod-shaped hemagglutinin (HA) and neuraminidase (NA) spikes (Betts, 1995). Influenza viruses are of three types A, B, and C. The typing

In order to better understand aging-associated diseases, it is first necessary to define what aging is. Aging is a complex, multifactorial process of harmful mutations in cells and tissues that are accumulated over time and result in an increased risk of disease and, eventually, death (Tosato, Zamboni, Ferrini, & Cesari, 2007, p. 401). Contrary to the belief that aging can be cured through medical advances, it is scientifically accepted that, while human life expectancy has increased, the human life span has remained largely unchanged for the past 100,000 years (Tosato et al., p. 401). Therefore, future developments in aging research ought to focus on addressing treatment and prevention of major aging-associated diseases that will

Microbiology traces the influenza viruses as enveloped RNA viruses from the Orthomyxoviridae family. Their genome has been identified as having a high mutation rate and they show increased antigenic diversity. Their core protein can be classified into three distinct types: A, B and C. Influenza viruses have two major antigenic surface glycoproteins embedded into their membrane: the hemagglutinin (HA) and neuraminidase (NA) which create the antibody response in humans4. Influenza types A, B and C can infect various mammals including humans, pigs, horses and both wild and domestic birds.

Two distinct lineages of H9N2 influenza viruses exist: North American and Eurasian lineages. The Eurasian lineage is composed of at least three sub-lineages. This lineage is divided into three major sub-lineages represented by their prototype strains: A/chicken/ Korea/38349-p96323/96 (Korean-like), A/duck/Hong Kong/ Y280/97 (Y280-like), and A/quail/Hong Kong/G1/97 (G1-like) [13, 23]. Throughout the second half of the 1990s, outbreaks resulting from H9N2 subtypes were reported in many countries, namely Germany, Italy, Ireland, South Africa, USA, Korea, China, and the Middle Eastern countries such as Saudi Arabia and Iran [4].

The virus was a unique combination of swine, bird, and human influenza viruses and its genetic composition was different from the human seasonal H1N1 viruses that were in circulation among people since

Throughout human existence, aging has been viewed as a large mystery and was thought to be a process that occurs naturally amongst all living organisms. It was discovered that senescence rates differ and there are species that exhibit negligible senescence. Studies involving longevity revealed that the FOXO family of transcription factor plays a large role in extending the lifespan of many different organisms, including humans. These transcription factors upregulate the genes involved in cell cycle arrest, oxidative stress, metabolism, and proteostasis, all of which are important in maintenance and quality control. When the functions of the transcription factors are conserved in organisms, lifespan is lengthened. Here, we will determine whether FOXO-dependent proteostasis impacts aging and how it impacts it. It remains unknown whether changes in FOXO expression or activity impact cellular quality control during aging. It is important to examine because proteostasis pathways

The way God created us as humans is a life cycle where eventually late adulthood comes with the biology of aging. Santrock (2013) describes five different theories of why humans age (p. 541). The evolutionary theory explains that aging is more of a natural selection process, and diseases occur in the elderly because they “would have been eliminated” if they were in younger people (Santrock, 2013, p.541). Cellular clock theory describes how cells get tired of dividing after they have been reproducing for so long (Santrock, 2013, p.541). Free-radical theory explains when “cells metabolize energy the by-products include unstable oxygen molecules known as free radicals” (Santrock, 2013, p.541). The unstable oxygen molecules can damage DNA and other structures inside the cell (Santrock, 2013, p.541). Mitochondrial theory describes how aging occurs because of the mitochondria essentially wearing out and becoming less efficient (Santrock, 2013, p.542). Mitochondria are the cell’s “power house,” and they convert energy inside the cell (Bailey, 2008). The last theory, hormonal stress theory, illustrates the effects of stress, especially long term stress, on aging (Santrock, 2013, p.542). Stress released hormones which depress the immune system making people more susceptible to disease (Santrock, 2013, p.542). There are many theories about why human’s age, and all of them may be true, but regardless aging is inevitable and so are its effects.

According to theory of aging, free radical interferes in this case. Aging is the apparently unavoidable decrease in physiologic function that happens after some time. At least four main theories of aging have been discussed that imply to clarify much or majority of the reason of biological aging:

Telomeres are directly correlated to the aging of a human body. Although some people might think that shorter telomere lengths are detrimental, the natural shortening of these telomeres are essential to healthy and normal aging. It is natural for cells to divide through mitosis, but each time cells are split telomeres are lost through the process. This is why the telomere maintenance system was evolved to protect the ends of chromosomes (Prescott, Kraft, & Chasman, 2011). Every time a cell is divided, its telomeres are weakened, and stress can accelerate this weakening, and biologically age the person. As a

Aging is the process of becoming older, as we age, multiple mutations occur that concern all the processes of aging well as it compromising a number of different genes. There are many theories of biological aging, such as the Cellular Aging Theory, Immunological Theory, and the Wear and Tear Theory. The Cellular Aging theory describes the process of aging in which cells slow their number of replication, thus giving each species a “biological clock that determines its maximum life span” and how quickly one 's health will deteriorate(Hooyman, 42). After a certain number of years, each cell which follows an apparent biological clock starts to replicate itself less, thus the specific individual or species slowly deteriorates. This theory gives

Causes of aging are very uncertain. Besides, there are several factors which predispose an individual to premature aging. Current theories suggest that this process occurs to due to cellular damage such as DNA oxidation by free radicals causing