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Immunology, Microbiology, and Epidemiology of HIV, Research Paper Example

Pages: 14

Words: 3915

Research Paper

Introduction

The human immune system exists as a complex network of biological functions and interacting cells, cell products, and cell-forming tissues that protects the body from pathogens and other foreign substances by distinguishing foreign tissue and neutralizing potentially pathogenic organisms or substances, destroys infected and malignant cells, and removes cellular debris (Immune system, 2002).  Comprised of multiple infrastructures, the human immune system includes the thymus, spleen, lymph nodes and lymph tissue, the skin and mucous membranes, stem cells, white blood cells, antibodies, and lymphokines (Immune system, 2002).   Exposure to viruses, such as an infectious disease like the HIV (Human Immunodeficiency virus), either during circumstances beyond individual control or through risqué behavior, can cause fatal disruptions in the functionality of the innate and adaptive abilities of the human immune system, causing uncontrollable microbial reproduction within the host.  This causes an immunosuppressive reaction that leaves the host susceptible to virulence in other forms and ultimately results in the death of the infected person without discretion.  This discourse will present the immunology, microbiological attributes, and current epidemiology of the HIV virus, concluding with a succinct synopsis of the most prevalent means of transmission of this incurable fatal infectious disease and the most effective means of avoiding contraction.

Immunology and Host Behavior of HIV

The HIV virus is an opportunistic infection that uses vertical transmission due to its narrow host range and stems from two major strains, HIV and HIV-2, which can be further divided into the groups of HIV (M, N, O and P) and HIV-2 (A–H), which can be further subcategorized into additional genetically unique circulating recombinant forms and unique recombinant forms of the disease (Jan 10, 2012; Peeters, Aghokeng, & Delaporte, 2010).  This virus is a highly infectious communicable disease that is spread through a direct exchange of bodily fluids, most often during sexual intercourse although blood to blood contact, such as through sharing needles for intravenous injection or blood transfusion can also transmit HIV.  Mothers infected with the HIV virus can also transmit the disease to their offspring during pregnancy, through the birthing process from their blood, or through their breast milk if they choose to nurse.  However, the HIV virus is not capable of penetrating the body’s first line of defenses, which includes the mechanical barriers, such as skin and the chemical barriers, like enzymes and lysozymes in saliva (Jan 13, 2012).  When the HIV virus is transmitted during sexual intercourse, it enters the bloodstream through mucous membranes lining the vagina, rectum, or mouth, where macrophages and dendritic cells on the surface of those mucous membranes bind to the virus and carry it into the lymph nodes (Bassett, 2011).  The lymphatic system naturally has an abundance of helper T or CD4+ T cells, which the virus uses for replication and to establish the infection (Bassett, 2011; Jan 13, 2012).

As in any other pathogenic invasion, when HIVenteres the body, it triggers an immune-biological response that initiates anti-HIV antibody and cytotoxic T cell production (Jan 13, 2012).  However, it can take the average newly infected human host anywhere from one to six months to produce measurable quantities of antibody naturally and the virus replicates at a rapid rate in the interim (Korber et al., 2001).  As the virus replicates, memory T (CD4+ and CCR5+ cells) are destroyed, which progressively weakens the immune system’s ability to respond to the viral infection, and replication increases the viral load, resulting in viremia and, eventually, the complete dissemination of the HIV virus throughout the body’s lymphatic and other systems (Jan 13, 2012).  Typically, the body’s natural immunological response to combat a virus eventually provides sufficient protection that eradicates the virus from the body, forming antibodies to the illness, which are the body’s notes on battle strategies for future use, but HIV replicates so swiftly that it manages to establish a chronic infection in the body before the natural defenses can create enough antibodies to fight the disease.  A chronic persistent infection occurs when a pathogen is able to successfully complete seven steps, which are:

  • maintain a reservoir, which is the area in which the virus can safely remain and multiply, by staying at undetectable levels in a susceptible host during the initial stages,
  • obtain mobility and the capacity to be transferred to another suitable host,
  • adhere to, colonize, and/or invade host cells,
  • initially evade host defenses,
  • complete the life cycle through reproduction or multiplication,
  • mechanically or chemically damage the host, and
  • leave the host and return to a new host or the reservoir (Jan 10, 2012)

The HIV is able to fulfill all of these requirements and the human processes in which the production of cytokines and cell divisions occur to regulate the immune response for protection also cause the HIV virus to replicate (Jan 13, 2012).  This manipulation of the body’s natural defense system causes such a swift turnover of CD4+ T cells that the result is a cataclysmic destruction of lymphatic tissues, which ultimately inhibits the body’s ability to form an immunological response to any invading substance, from viruses to parasites (Coiras, López-Huertas, Pérez-Olmeda & Alcamí, 2009; Saubolle, 1998).  Cytotoxic lymphocyte production mirrors the increase of HIV virus cells in the blood and HIV particular CD4+ T cells may be particularly vulnerable to invasion from HIV virus cells (Jan 13, 2012).   The HIV virus will also bind to a glycoprotein expressed on dendritic cells called CD-SIGN or travel to HIV virus-bearing dendritic cells that have been activated to helper T cell areas of lymph nodes and specifically infect helper T cells with HIV peptides (Corais et al., 2009).   Reductions in HIV specific helper T cell numbers may lead to diminished galvanization and endurance of cytotoxic CD8 T cells and also produce a partial initiation of CD8 T cells that would be able to eradicate HIV diseased cells, causing a decreased ability to destroy virally infected cells (Corais et al., 2009)).

The rapid loss of memory helper T cells and the immune system’s inability to replace these corrupted cells causes increasing immunodeficiency and the high mutation rates of the HIV also allow virus to evade modulated responses of the body’s debilitated immune system (Saubolle, 1998).  Since the body’s primary source of mucosal immunity is in the intestinal immune system, the HIV virus quickly infects and destroys these cells, even in in host individuals that are currently in treatment regimens (Korber et al., 2001).  The rate in which the virus load reaches critical mass and transitions from HIV virus into full blown AIDS (Acquired Immunodeficiency Syndrome) is solely dependent upon how well the host body can replace T cells consumed by the virus as well as how swiftly the replication rate is accompanied by viral turn-over and how well they tolerate pressure for change and actual change.  The ability of the HIV virus to execute relatively large insertions and deletions causes the virus to rapidly generate radically divergent viral strains, making the virus particularly resistant to vaccinations due to the variations in the subspecies varieties (Saubolle, 1998).  Although an HIV viral infection begins with a homogeneous viral population, as all viral infestations do, over the course of a typical infection, strains mutate to alter more than 10% of their DNA structure, creating the possibility of unique classifications of the virus within each new host (Korber et al., 2001).

The methods for diagnosis vary from simple blood tests to complex genetic analysis, depending on the specificity desired.  Diagnosis through venipuncture for pooled qualitative HIV RNA or quantitative RNA has the potential to identify both acute and chronic HIV infections that are otherwise missed by standard HIV testing algorithms (Bassett et al., 2011).  Another common test that can be done from blood analysis is the Western blot (WB), and the rapid HIV test (Bassett et al., 2011).   However, these methods are not always reliable and can deliver false positive or false negative results.  Although newer methods of testing, including direct antigenic/genetic material detection by enzyme immunoassays, monoclonal fluorescent studies or genetic probes, and molecular amplification systems are being used more frequently in lieu of the aforementioned approaches to diagnostics, the amplified delicacy of the test methods frequently interferes with their specificity and escalates the difficulty interpreting the result obtained from these testing techniques (Saubolle, 1998).

Microbiological Agents of HIV

The successful use of vaccination to diminish the occurrence of Polio has elected vaccination as the eradication method of choice for infectious diseases (Feb 10, 2012).  The aim of a vaccine is to exploit the inherent memory capabilities of the of the body’s immune system to combat illness by stimulating the production of antibodies and memory B‐ and T‐cells that will respond to disease‐causing organism through the introduction of foreign pathogens as similar as possible to the antigen of the disease‐causing organism (Feb 10, 2012).  This will induce the natural immunological response, which will be to form antibodies, thus teaching the body how to combat the intended illness.  However, the complex abilities of the HIV virus to mutate into unique genetic strains has led to the failure of several HIV vaccine clinical trials, which emphasizes the urgent demand for the innovation of supplementary varieties of pre-emptive devices to impede the sexual transmission of HIV through the use of microbiological devices (Wilson, 2006). Microbicides are technological instruments that can be rendered in the form of topical gel applications, long-term contraceptive implants, or oral/injectable pharmaceuticals agents that can be engineered to disrupt one or more steps in the necessary for the HIV virus to establish itself within its host, inactivate the virus completely, or increase the user’s immunity and can be used by males or females (Kiser, 2008).

They can also be designed to remain present in the vagina for as short as a day and up to a month, enhancing the microbial ecology of the vagina to repel infection and functioning in contraceptive or non-contraceptive manner, depending on the intent of its design (Kiser, 2008). Microbiological sciences can be used to identify and destroy a specific infectious agent using the indicated technique to perform the test (Pathology, 2009).  The testing techniques can include antigen detection, direct fluorescence microscopy, infectious agent detection and nucleic acid probe and a single technique must be used for each infectious agent to ensure that the presumptive identification of all microorganisms is accurately classified, according to the colony morphology, growth on selective media, gram stains, or up to three tests other tests, such as catalase, oxidase, indole, and urease (Pathology, 2009).  Definitive identification of microorganisms is described as recognition of the genus or species level and would require additional tests, like biochemical panels and slide cultures and, if other research involves molecular probes, chromatography, or immunologic techniques, they should be coded individually, in accordance with to conclusive documentation routines (Pathology, 2009).

There are many obstacles that have obfuscated endeavors to cultivate a safe and effective microbicide against HIV, such as the focus on women-controlled microbicides as part of the global initiative to battle the endemic, which has made the endeavor all the more dire (Kiser, 2008).  The novelty associated with this relatively new science of microbicides and the numerous unknown parameters that challenge the identification and development of a successful microbicides, which include defining the best contrivance design to optimize user acceptability, selecting the best drug or combination of drugs to fight the complexly unfamiliar biology of HIV, and intuiting whether the product design will necessitate changes in the sexual behavior of the user (Kiser, 2008). One corporation currently attempting to develop a microbiological cure for HIV is Sangamo Bio-Sciences, and they have recently pioneered a technique for cutting the DNA strands of genes in judiciously designated spots (June & Levine, 2012).  Exceedingly more efficient and diverse than other tactics, this method was able to hone in on a explicit gene sequence designated for editing using zinc finger proteins, which are inherent molecules that fuse to DNA during gene transcription, the manner in which the data contained in the DNA molecule is converted into the RNA molecule necessary to synthesize a programmed protein (June & Levine, 2012).   Homo sapiens naturally create around 2,500 distinct zinc finger proteins, with each protein specific to a singular nucleotide sequence on the DNA molecule, and the complexity of these considerations, as well as a multitude of others, have resulted in a number of recent unsuccessful microbicide clinical trials just as there were with the vaccine trials, (Kiser, 2008).

Scientists devised a method to artificially construct zinc finger proteins that can latch onto any particular DNA sequence of assigned, which has spawned the suggestion that the Sangamo corporation fashion a tailored set of DNA scissors by first making zinc finger proteins that will attach to either end of any sequence that needed to be deleted and then, company scientists would add a second protein to each of these proteins, an enzyme called nuclease, which can cut DNA strands in two (June & Levine, 2012).  The zinc finger would detect the sections of the DNA to cut, and the nuclease would slice the genetic material (June & Levine, 2012).  Through the development of the right pairs of zinc fingers, the Sangamo corporation could aim at a particular section of the CCR5 gene, like the section contaminated by the HIV virus, without accidentally damaging other genes (June & Levine, 2012).  Once the customized zinc finger nucleases was attached to the DNA sequence in question, the cell’s healing mechanism would initiate, and the device would distinguish the separation and repair the severed pieces of DNA, thus curing the infection (June & Levine, 2012).  While this is theoretically the way this technology is supposed to work, the trials have not demonstrated such ease of function, which has kept an actual cure for HIV an elusive goal for both vaccine and microbiological trials.

Environmental Demographics and Epidemiology

Epidemiology is the study of the dissemination and causal factors related to specific health issues and events in quantified populations and the application of these details are typically used to assess the degree of contamination within a populace (Jan 23, 2012).  The epidemiological details can also be used to:

  • Assessing the risks of exposure for a developing disease based on needle sharing patterns among injection drug users (Jan 23, 2012)
  • Identify the cause of new syndromes of HIV (Jan 23, 2012)
  • Study the natural history and prognosis of the disease (Jan 23, 2012)
  • Deciding whether possible management strategies will be effective, including antiretroviral drugs and their success in preventing the mother-to-child-transmission of HIV (Jan 23, 2012)
  • Discerning appropriate disease prevention strategies that align with the community and assessing if they are helpful (Jan 23, 2012)
  • Recognizing the health service needs and trends within the community, including the use of antiretroviral treatment services (Jan 23, 2012)
  • Offer a basis for healthy public policy adjustments, including dietary changes and health practices (Jan 23, 2012)
  • Tracing the origins of outbreaks to inform and educate those affected (Jan 23, 2012)

It is estimated that approximately 0.8 percent of people worldwide, between ages 15-49, are infected with HIV, equating to a prevalence in all world regions of one percent or lower, with the exception of sub-Saharan Africa where the prevalence is five percent (Bongaarts, et al., 2008).   However, this is not a constant, as prevalence levels range from a fraction of 1 percent in several countries in Western Africa to above 15%in some countries in Eastern and Southern Africa (Bongaarts, Buettner, Heilig, & Pelletier, 2008).  The incubation period refers to the timeframe between which the HIV virus enters the body and when the first symptoms of infection begin to appear, and the first stage of HIV virus is when the virus travels through mucous membranes and into the cells, causing symptoms, which can occur as early as 2 weeks after contact with the virus and as long as seven to ten years following initial contact (Saubolle, 1998).  The virus can be diffused through the eyes, the gastrointestinal tract and, the central nervous system, which was recently recognized, and recent studies have revealed a relationship between a high systemic Cytomegalovirus (CMV) load and advanced HIV diseases (Saubolle, 1998).  CMV load also seems to forecast the onset of disease, reaction to treatment, and disease prognosis, although not many patients with CMV retinitis have minute viral loads, and a variety of methods have been implemented to demonstrate the connotation between viral load and disease progression, including CMV antigenemia assay, whole blood PCR, and plasma PCR, but no single method has been shown to be better than another at this time (Saubolle, 1998).

According to the Center for disease Control (CDC) (Number, 2008), from 2003 through 2006, the projected figure of HIV cases in the 33 states with private name-based HIV infection reporting remained stable, but the total amount of new of persons living with HIV increased steadily to 491,727.   The disparate bearing of HIV among gay and bisexual men (MSM) in the United States is more than 44 times that of other men and more than 40 times that of women, whereas the range was 522-989 cases of new HIV diagnoses per 100,000 MSM vs. 12 per 100,000 other men and 13 per 100,000 women (CDC: Number, 2008).  Furthermore, gay and bisexual men comprise the bulk of new HIV infections, and the CDC is attempting to develop more concise estimates regarding the rate of infection among MSM by race and age, as well as among injection drug users (HIV rate, 2010).  Ultimately, such information can be applied to better appraise nationwide and indigenous methods to HIV and STD avoidance to guarantee that labors are getting to the people in utmost need.   There are a wide variety of complex issues adding to the high instances of HIV among gay and bisexual men, which include a high propensity for HIV and other STDs among MSM, which intensifies the risk of exposure to the disease, and limited access to prevention services (Wilson, 2006). Other influences include nonchalance regarding their risk for contracting HIV, particularly among young gay and bisexual men; the strain of constantly upholding anodyne actions with every sexual encounter over a lifetime; and lack of awareness about the symptoms and transmission of HIV, including the dangers of contagion from oral sex (Kilmarx, 2009).  Compiling on these factors, issues like homophobia and stigma can prevent MSM from pursuing prevention, getting tested, and seeking treatment services, which makes the risk of HIV diffusion through receptive anal sex is much greater than the risk of transmission via other sexual activities, especially since some gay and bisexual men rely on deterrence tactics that are less effective than consistent condom use (Kilmarx, 2009).

Historically, HIV epidemics have been considered concentrated if the HIV prevalence in the general population was below one percent and generalized if such pervasiveness in the general population exceeded one percent, but pulation-based surveys have demonstrated that HIV infection within the general population has been overestimated in many cases (Wilson, 2006).  Globally, the percentage of people with HIV infection who are women has remained stable at 50% for several years, with the estimates for adolescents and young adults aged 15–24 years account for 45% of new HIV infections globally (Kilmarx, 2009). However, the international statistics hide significant indigenous and provincial epidemiologic heterogeneity, including promising decreases in frequency in some countries, notably in sub-Saharan Africa, while contamination rates increased in other areas, like Eastern Europe and central Asia (Kilmarx, 2009).  It should also be noted that statistical evaluations have reported that global and key regional estimates in 2007 were lower than those published in 2006, due largely to new statistics indicating that former estimations were too high, explicitly, results from numerous population-based assessments largely indicating lower HIV prevalence’s than those from sentinel site surveillance (Kilmarx, 2009).

Conclusion

Exposure to an infectious disease like the HIV virus can cause fatal disruptions in the functionality of the innate and adaptive abilities of the human immune system, causing uncontrollable microbial reproduction within the host that typically results in an immunosuppressive reaction that leaves the host susceptible to virulence in other illnesses, ultimately resulting in the death of the infected person without prejudice.  Treatment through antiretroviral therapy will not benefit everyone living with HIV immediately and it is vital tyo stress the importance of maintaining protective behavior, and the value of knowing one’s HIV status, as treatment eligibility depends on a range of factors including viral load, immune suppression, individual readiness to start, and the presence or absence of HIV-related disease, among other variables (Aggleton, Yankah, & Crewe, 2011).  Additionally, there are extreme disparities in the epidemiology and preventative methods regarding HIV and the treatment and care of patients from underrepresented and underserved populations, particularly African Americans and Hispanics. The demographics of the HIV epidemic indicate that there is a disproportionate impact of HIV infection and transmission on racial/ethnic populations, yet investigators from socially disadvantaged racial/ethnic groups remain significantly underrepresented (Gable, Gostin, & Hodge, 2008).  In many countries, HIV infected women are subject to laws and informal practices that restrict their reproductive freedom.  Legislation should be grounded in human rights and explicitly provide safeguards against discrimination based on HIV status, gender, or reproductive status (Gable, Gostin, & Hodge, 2008).  The international community and many countries recognize the positive correlation between respecting human rights and preventing HIV, as exemplified in the 2001 Declaration of Commitment on HIV (Bongaarts et al., 2008).  Education is key to prevention, including prevention and treatment options, as the largest epidemics occur in populations where multiple and concurrent partners are relatively common, where condom use and male circumcision are rare, and where ulcerating sexually transmitted infections are prevalent, although in the absence of most of these factors, the HIV virus has difficulty establishing and sustaining itself, and the HIV prevalence rate is typically less than one percent (Bongaarts et al., 2008).

References

Aggleton, P., Yankah, E., & Crewe, M. (2011). Education and HIV/AIDS-30 years on. The Guilford Press, AIDS Education and Prevention, 23(6), pp.495-507

Bassett, I.V. et al. (2011). British HIV Association Screening for acute HIV infection in South Africa: finding acute and chronic disease. HIV Medicine, 12, pp.46-53 doi: 10.1111/j.1468-1293.2010.00850.x

Bongaarts, J., Buettner, T., Heilig, G., & Pelletier, F. (2008). Has the HIV Epidemic Peaked?. Population And Development Review, 34(2), 199-224.

CDC: number living with HIV on steady rise: new cases stable, survivors increasing. (2008). AIDS Alert, 23(6), 70-72.

Coiras, M., López-Huertas, M., Pérez-Olmeda, M., & Alcamí, J. (2009). Understanding HIV latency provides clues for the eradication of long-term reservoirs. Nature Reviews Microbiology, 7(11), 798-812. doi:10.1038/nrmicro2223

Gable, L., Gostin, L., & Hodge, J. r. (2008). HIV/AIDS, reproductive and sexual health, and the law. American Journal Of Public Health, 98(10), 1779-1786. doi:10.2105/AJPH.2008.138669

HIV rate 44 times higher in gay, bisexual men: CDC: HIV infections a rite of passage?. (2010). AIDS Alert, 25(4), 42-43.

Immune system. (2002). The American Heritage Science Dictionary. Retrieved from Dictionary.com website: http://dictionary.reference.com/browse/immune system

June, C. & Levine, B. (Mar2012). Blocking HIV’s Attack. Scientific American, 306(3). Retrieved from Academic Search Premier.

Kiser, P. (2008). Simple but Sophisticated: Microbicide Technologies to Fight the Global HIV Pandemic. Brown Journal Of World Affairs, 15(1), 135-143.

Korber, B. et al.  (2001). Evolutionary and immunological implications of contemporary HIV variation. The British Council, British Medical Bulletin, 58, pp.19-42. Retrieved from http://bmb.oxfordjournals.org/

Pathology: microbiology. (2009, May).

Peeters, M. M., Aghokeng, A. F., & Delaporte, E. E. (2010). Genetic diversity among human immunodeficiency virus-1 non-B subtypes in viral load and drug resistance assays. Clinical Microbiology & Infection, 16(10), 1525-1531. doi:10.1111/j.1469-0691.2010.03300.x

Saubolle, M.A. (1998, September 18). The clinical microbiology laboratory in the diagnosis and monitoring of opportunistic infections in HIV-infected persons. 1998 Conference on the Laboratory Science of HIV, Good Samaritan Hospital and Medical Center, Phoenix, AZ.

Stoff, D., Forsyth, A., Marquez, E., & McClure, S. (2009). Introduction: the case for diversity in research on mental health and HIV/AIDS. American Journal Of Public Health, 99S8-15. doi:10.2105/AJPH.2008.153536

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