In addition, prospects or HIVE vaccine will be briefly examined as well as the potential for antiviral drugs. The epidemic of HIVE disease and AIDS is now well into its third decade. It has garnered more attention than any new disease to appear in recent history, and it continues to spread. Acquired immunodeficiency syndrome, better known as AIDS, threatens significant portions of the human population. Although the 1 sass have witnessed major advances in treatment, HIVE infection remains an ultimately fatal disorder. Structure of HIVE HIVE is a typical retrovirus in size and shape. Two antigenic globetrotting characterize its envelope.
The larger globetrotting, named guppy, is the primary attachment molecule of HIVE to four kinds of cells: helper T cells, cells of the macrophages lineage, smooth muscle cells, and dendrites cells (Hung, L am, Chary, Tang, Axing et al. , 2007). Its antigenic changes during the course of prolonged infection, making an effective antibody response against it difficult (Hung, Learn, Chary, Tang, Kiang, et al. , 2007). The smaller globetrotting, gaps , promotes fusion of the viral envelope to a target cell and the HIVE virus releases its Sara genome from the sapid into the cell’s cytoplasm (Chou, Lu, Tan, Kiang ; Chin, 2011).
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The effects of these structural characteristics – antigenic variability and the ability to fuse with host cells – interfere with clearance of HIVE from a patient (Kong, Wyatt, Robinson, et al. (1998). The infectious cycle of HIVE infection AIDS develops as the end result of long-term infection with one Of two closely related viruses, HIVE-I and the less common HIVE-2 (Porter ; Kaplan, 2004). The two viruses are very similar structurally and cause identical clinical manifestations (Frame ; Brander, 2007). They are both single-stranded RNA retroviruses, so named because they can transcribe their viral RNA into DNA (Ukrainians, 1994).
For HIVE infection to occur, the virus must be absorbed into the bloodstream. Then surface protein on the virus outer wall, or envelope, bind to receptors on the outer surface of CDC+ cells, including T-lymphocytes (Hung, Lam, Chary, Tang, Giant et al. , 2007). After attachment, the viral RNA enters the host cell and is transcribed by a viral reverse transcripts enzyme into double-stranded DNA( Kong et al, 1998). This viral-encoded DNA is transported into the cell nucleus, where it is incorporated into the host-cell DNA.
The viral DNA then directs the host cell to produce HIVE-specific proteins (Frame ; Brander, 2007). These proteins, according to Frame ; Brander (2007) must be cut, or cleaved, by another viral protein, called a protease, into segments. The segments are then assembled into infectious viruses, which either bud off from the host cell or are released on cell death (Porter ; Kaplan, 2004). The mechanism of viral replication is important to understand because approaches to treatment are based on the viral life cycle (Porter ; Kaplan, 2004).
HIVE infection inflicts damage to the host immune system through the progressive loss of CDC+ T-lymphocytes (Porter ; Kaplan, 2004). The homophobes, termed helper/suppressor cells, are critical in modulating the normal immune response. At first, the body’s immune response keeps up with the active viral replication (up to 1 billion viral particles are produced each day, even in asymptomatic HIVE-infected individuals) by replacing the lost CDC+ cells (Porter & Kaplan, 2004). Over time, however, the body’s ability to replace the lost CDC+ T-lymphocytes wanes, and progressive immunodeficiency results.
This leaves the host susceptible too range of unusual infections (referred to as opportunistic infections) and cancers, which electively represent the clinical disorder termed AIDS (Frame ; Brander, 2007). Pathology and disease HIVE transmission requires contact with body fluids containing infected cells or plasma. HIVE may be present in any fluid or exudates that contains plasma or lymphocytes, specifically blood, semen, vaginal secretions, breast milk, saliva, or wound exudates. Although, theoretically possible, transmission by saliva or droplet nuclei produced by coughing or sneezing is extremely rare, if it occurs.
HIVE is not transmitted by casual contact or even by the close nonsexual contact that occurs at work, school, or home. The most common means of transmission is direct transfer of bodily flu ids either through sharing contaminated needles or sexual relations. HIVE infection passes through predictable stages, during which the body’s immune system is gradually undermined (Frame & Brander, 2007). Although the duration of the infection varies, depending on the person’s health and behavior, there is a gradual depletion of cells in the body that are crucial to its defense against disease-causing agents (Hung, Lam, Chary, Tang, Axing, et al. 2007). Soon after contracting HIVE, some people develop a fever, swollen glands, fatigue, and perhaps a rash (Porter ; Kaplan, 004). This is called primary HIVE disease. These early symptoms usually disappear within a few weeks as the body manages to ward off the infection with its immune defenses, and there may not yet be enough antibodies to show a positive HIVE test (Frame ; Brander, 2007). The second stage is called chronic asymptomatic disease, and is characterized by gradual decline in immune cells even though there are no particular disease symptoms (Porter ; Kaplan, 2004).
Eventually, most people infected with HIVE begin to experience chronically swollen lymph nodes, although they may have few other symptoms (Hung, Cam, Chary, Tang, Axing, et al. 2007). As the infection progresses, there is a continual drop in the number of immune cells in the body. The individual becomes increasingly vulnerable to opportunistic infection, in which disease-causing organisms normally present in the environment become able to attack the person by taking advantage of the weakened resistance (Hung, L am, Chary, Tang, Axing et al. , 2007). This is the third stage, and is called chronic symptomatic disease.
One of the most common infections in this stage of HIVE disease is a yeast infection of the mouth called thrush (Porter ; Kaplan, 2004). There may also be infections of the skin and moist inner membranes of the body, according to Porter ; Kaplan (2007). In addition, many of the diseases associated with the loss of immune function in AIDS are nonlinear infections in other patients, but AIDS patients cannot effectively resist them (Porter ; Kaplan, 2004). Diseases such as Kapok’s sarcoma, disseminated herpes, taxonomists, and Pneumatics pneumonia occur rarely except in AIDS patients (Hung, Cam, Chary, Tang, Kiang, et al. 2007). Vaccines or prospects for HIVE vaccine? Viral diseases can sometimes be prevented or brought under control by connation. Vaccines take advantage of the body’s ability to “remember” a disease-causing agent. They involve introducing a harmless form of the germ into the body, so that the immune system is fooled into working as if it were being attacked by the actual germ and develops necessary antibodies to ward off later infections. The search for an HIVE virus has been a top priority since 1984, and experts still rank such a vaccine as the most urgently needed in the world (Girl, Gene, ; Winner, 2004).
There have been several major complications that make the search a difficult one. First, HIVE seems to be able o hide in cells by installing its genes within the genes of the cell, thus making it difficult to identify specific immune responses that can prevent infection and limit disease progression (Mustache, 2000). Second, although scientists have developed a vaccine that protects monkeys from SIVA disease they have not been able to translate this success into an effective vaccine for humans due to structural and antigenic differences (Voyage, et al. 2003).
Third, since HIVE infection is so dangerous, experimental trials for a vaccine with humans have had to proceed with the utmost caution (Robinson, 2002). In such trials, a substantial number of at-risk people are given the vaccine, and their rate of infection is compared to a control group of persons who have not received the vaccine (Robinson, 2002). Finally, there are concerns that it may be difficult to protect the privacy of individuals who participate in the trials, and that it will be difficult to provide liability coverage in case experimental vaccines cause injury or disease (Rose et a’, 2001).
Some scientists have speculated that developing a vaccine to ward off HIVE disease and AIDS may simply be impossible, while others are more helpful (Mustache, 2000). Since there are different strains of HIVE, there is some concern over whether several vaccines will have to be developed to protect people from AIDS (Robinson, 2002). Currently, there is a quest for the development of novel vaccine approaches. The use of live recombinant vectors and plasmid DNA inhomogeneous are among the most promising approaches (Girl, Eugene, & Winner, 2004; Flynn, Fortran, Harrow, et al. 005). Thus, progress in developing a vaccine against HIVE still has been disappointing. Potential for antiviral drug? Several new principles of treatment for HIVE infection emerged in the id-1 sass. New methods to quickly measure the effects of drugs on HIVE in the blood, ii, suppression of plasma HIVE RNA levels, and a better understanding of the rapid production of HIVE, even in the clinically inactive stages of infection, have changed the approach (Creases & Element, 2007).