The dengue virus belongs to the family of Flaviviridae, genus Flavivirus. It is also known as Arbovirus ( arthropod- borne virus) as it belongs to group of virus that is transmitted by an arthropod or mosquito ( Medical Microbiology; pg 554). The dengue virus is of the size of 40- 65 nm in diameter, roughly spherical and has outer lipid envelope. It is a positive stranded RNA genome made up of 10 000 nucleotide base pairs. The RNA genome contains a single open reading frame that encodes a precursor polyprotein, which is co- and post-translationally cleaved into three structural (C, prM and E) and seven non-structural (NS1, NS2A, NS2B, NS3, NS4A, NS4B, NS5) proteins. The core of the virus is surrounded by nucleocapsid which is a structure that …show more content…
The pathogenesis of this self limiting dengue can be broadly divided into 2 categories, that is:
(a) The general pathogenesis of the virus, beginning from the entry to the body till the cause of fever.
(b) The dengue virus replication and infectious cycle which occurs in the cell
5.2.3.1 General pathogenesis of dengue fever
When a mosquito carrying dengue virus bites a person, the virus enters the skin together with the mosquito's saliva. It binds to and enters white blood cells (specifically the immature dendritic cell or Langerhans cell located in the skin), and reproduces inside the cells while they move throughout the body. The white blood cells respond by producing a number of signalling proteins, such as cytokines and interferon, which are responsible for many of the symptoms, such as the fever and severe pains. However it is to be noted that this fever is actually self limiting. The overview of the pathogenesis of the virus is illustrated in Figure 2 and Flowchart
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neutralizing antibody and non neutralizing antibody. When the same individual is infected with different dengue serotype, DHF or DSS results. (For example, he is infected with DENV 1 and then re infected by DENV2). This is because the virus infects the body cells following the general pathogenesis (See under Pathogenesis of Dengue Fever) and another pathway is the ADE mechanism. The ADE mechanism is nothing but the non neutralizing antibody will ‘help’ the virus to gain entry into the cell (Figure 4). Thus, this will result in higher number of target cell being infected which in turn could lead to a higher viral load which was observed in many studies ( PubMed; Oct 2009; Dengue virus pathogenesis: An Integrated View; Byron E. E. Martino et
The capsid carries DNA or RNA1 which give the virus its unique features. In this state the virus is metabolically inert, or it doesn’t use any of its resources to make energy. 1 - Ribonucleic acid: it performs as a messenger for the DNA cells; it manufactures the proteins for living cells using the DNA’s genetic information. When were viruses discovered and who discovered them?
To identify if the disease is a virus, there must be evidence shown that the cells do not undergo binary fission; they create new particles like an assembly line. Another trait of a virus is they have a one, single nucleic acid, whether that be DNA or
The following pages show the effects of the illness and what measures have been taken. The Virus Itself Ebola has many ways of destroying one’s body. The virus is also so complex and confusing that scientists have to compare it to other viruses that they do know about. Preston (1995) points out, “The virus is related to diseases like mumps and rabies
The monkeys came in contact with the virus and then transmitted it to
The cell was wall-to-wall with worms. Some parts of the cell were so thick with virus they looked like buckets of rope. There was only one kind of virus that looked like rope. A filovirus. He thought, Marburg.
The Sudan Virus was first discovered in South Sudan in nineteen seventy-six, where it was described as “Ebola Hemorrhagic Fever” but classified as SUDV. Bats were suspected to harbor the virus because of the distantly related filo virus, MARV. MARV has been isolated from bats, but no reservoir host has been positively identified. As well as being unclear on how SUDV was introduced into the human
A rash starts on the face and upper neck, spreads down the back and trunk, then extends to the arms and hands, as well as the legs and feet. After about 5 days, the rash fades in the same order in which it appeared. The virus can be spread from four days before through four days after the rash
The clip that I chose to use is the case of the Zika virus. I am speaking on the 5 case of the Zika virus found in Miami. The Zika virus has arrived in the United States, with mosquitoes spreading the virus in two Miami-area neighborhoods and the CDC advising pregnant women to avoid those areas. Pregnant women who have traveled to the Wynwood area of Miami or a section of Miami Beach should see their doctor about getting tested, the CDC says. Pregnant women and their partners who live in the areas or must travel there should take steps to avoid mosquito bites.
This is when a virus attaches to a cell, injects its DNA into it, the cell starts making lots of new viruses, and eventually the cell breaks, releasing new viruses into the bloodstream.
Once inside, the virus basically hijacks the cells living organelles and masquerades itself as pieces of cellular DNA. From there, DNA code is transcribed into RNA messages which are translated into individual viral proteins. Then the virus components are assembled into thousands of new viruses (Crawford, 2011). Thus infecting the host and becoming the cause of many life threatening diseases. I’ve chosen yellow fever as my research topic for several reasons.
West Nile Virus (WNV), a mosquito-borne pathogen is a relatively new disease that has drawn a good deal of attention since it first arrived in New York City in 1999. Since the potentially fatal neurological disease was first found in New York, the disease has rapidly spread to all 48 of the continental United States and Canada. Outbreaks of WNV have even been reported in parts of South America, although the numbers of reported outbreaks are far fewer than what the United States has experienced. Between 1999 and 2015 The Center for Disease Control and Prevention (CDC) reported 42,000 cases of West Nile Virus and 1700 resulting deaths in the United States (CDC, 2015). Although the spread of West Nile Virus has been rapid in the US, the origin
When a foreign substance invades the body it detects many types of cells to try to verify them. Those cells trigger the B lymphocytes and produce antibodies that specialized proteins that locks specific antigens. Once they produce they stay so the immune system encounters that antigens again. So the antibodies will be ready to do its job. If someone gets sick with something they usually won’t get sick from it again.
In an immunologically naïve host, viruses attach to the host cells (Tortora, & Funke, 2013). Adaptive immunity is slower to respond than innate immunity it does have a memory component is a function of the immunological system. The immunological system is able to recognize specific antigens and react in such a way that the host generates antibody-mediated immunity (AMI), cell-mediated immunity (CMI), or both. Adaptive immunity is the body’s third line of defense. An example is lymphocytes (T cells and B cells).
It is constituting of 2130 coat protein molecules and a single-stranded RNA of 6400 bases. It’s rod like structure is assembled into a helix using the coat proteins and they form a hairpin structure(5,6). The protein monomer has 158 amino acids and assembled into four main alpha-helices that are joined to the central axis of the virus. The virion is 18 nm in width and 300 nm in length and a 4 nm core inside it(in the central part) (5,6,7). The TMV genome consists of 6.3-6.5 kb single stranded RNA and has a 3’ end which a t-RNA like structure and the 5’ end cap is methylated(8).
Malaria is the most common disease in third world countries with a tropical climate; the disease is caused by a parasite called Plasmodium, which is transmitted through the bites of infected mosquitoes. In the human body, the parasites multiply in the liver, and then infect red blood cells. Symptoms of malaria include fever, headache, and vomiting, and usually appear between 10 and 15 days after the mosquito bite. If not treated, malaria can quickly become life-threatening by disrupting the blood supply to vital organs. In many parts of the world, the parasites have developed resistance to a number of malaria medicines.