Reasons Why Infection with Human Immunodeficiency Virus (HIV) is hard to Cure

Posted: August 26th, 2021

Reasons Why Infection with Human Immunodeficiency Virus (HIV) is hard to Cure

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Table of Contents

Introduction. 3

Epidemiology of HIV Infections in the United Kingdom.. 3

Pathophysiology of HIV Infection. 4

Reasons It Is Hard To Cure HIV.. 5

The Virus Readily Mutates. 6

Immune System is Impaired. 7

Conclusion. 7

Reference List 9

Reasons Why Infection with Human Immunodeficiency Virus (HIV) is hardto Cure

Introduction

Human Immunodeficiency Virus (HIV) is among the class of lentivirus, which causes HIV infections. Lentivirus isa class of retroviruses that contribute to deadly chronic diseases that are characterized by long periods of incubation in humans (1). Other groups of animals that host lentiviruses include apes, goats, cows, sheep, and cats. Recent studies have discovered that these viruses are found in lemurs, monkeys, ferrets and rabbits. HIV is the most known lentivirus in the world. Once infected, the infection leads to a condition referred to as acquired immunodeficiency syndrome (AIDS) (1). The presence of this condition affects the immunity system of the body, thereby giving a chance to other opportunistic and life-threatening infections as the immune system continues to fail. Notably, AIDS can only be treated by treating the infections of HIV (1). However, HIV cannot be killed easily because of several reasons. The subsequent sections discuss about the reasons it is hard to cure HIV.

Epidemiology of HIV Infections in the United Kingdom

The population of people affected with HIV in the United Kingdom is relatively small. According to 2017 data on the prevalence of HIV and AIDS, it was found that there are about 101,600 people infected with HIV, translating to 1.7 percent per one thousand (1,000) people between the ages of 15 years to 74 years(1). Subsequently, about 4,364 individuals had been diagnosed with HIV, which is steadily decreasing over the years. The situation is attributed to declining in new diagnoses among bisexual and gay groups, which are among the most affected by HIV in the country (1). In 2015, the prevalence of HIV infections among these groups was about 70%. However, by 2017, the prevalence rate has dropped by almost a third to about 28%.Regardless of the decline, the 2017 data report on diagnoses still reveals that bisexual men, gay and MSM accounted for about 53% of new infections while heterosexual women and men accounted for 24% and 19% respectively(1). Moreover, among the black African women and men, they accounted for about 38% of new infections in the UK. The following chart displays a trend in HIV and AIDS over the period from 1998 to 2016.

Figure 1: New HIV Diagnosis and AIDS prevalence in the UK in 1998 and 2016(1)

From figure 1, HIV diagnoses were increasing at a high rate from 1998 until 2005. The rate of diagnosis began to decline gradually over time. Equally, the trend in AIDS diagnosis has been declining over the period, with the lowest reported in the year 2016. However, mortality rates remain on a gradual increase. The situation is attributed to the lack of a cure for diseases (2). Moreover, the condition is likely to reduce overtime, as there isa reduction in the rate of new diagnoses in the country. Besides these efforts to curb the condition, HIV remains prevalent among various sections of people, such as men who engage in sex with other men, transgender and black African women and men (2). Hence, the self-sustainability of the virus is strong enough within the society as it continues to adapt uniquely across the different environments.

Pathophysiology of HIV Infection

Once a human is infected with HIV, there is progressive destruction of the immune system predominantly by damaging the CD4++ T-helper lymphocytes. Once these cells are eliminated, opportunistic infections follow, which becomes frequent to the affected individual (2). Besides, the virus damages somebody organs such as the white matter in the brain. The entry of AIDS is an indication of the advanced stage of HIV infection, which is ultimately fatal (3). The duration between infection and death for people affected with HIV depends on medical management. Hence, the affected person is likely to go for over fifteen years but in the UK, the average period is twelve (12) years.

Early infections mostly affect the lymph nodes and the meninges. In the late stages, most patients experience persistent generalized lymphadenopathy (PGL). PGL consists of florid hyperplasia in the lymph node tissues that result in the enlargement of the lymph nodes and salivary glands. According to Lucas (6), the situation spontaneously regresses after which a period of clinical latency is followed before the development of AIDS. Currently, however, there are changes in the pathological spectrum in infections of HIV as the virus continues to spread into diverse communities(4). Advances in HIV drugs are also a key contributor to the changing nature of the virus infection because of mutation. Besides, opportunistic infections for patients affected with HIV infections are based on the environment one is exposed to. Similarly, the environment or exposure also affects the rate at which the immunity system declines once an individual is affected with the virus (4). Hence, this requires unique countermeasures that are specific to a given environment for successful control of the virus since the variation in pathological determines the individuals’ ability to be affected by the infection

Reasons It Is Hard To Cure HIV

The primary factor as to why it is hard to cure the HIV infection is the fact that the virus is highly resilient against the natural immune responses and other therapies (5) Accordingly, the reasons that contribute to difficulties in destroying the virus are discussed in the following sections;

The Virus Readily Mutates

The ability to mutate quicklymakes the virus elusive and hard to fight. HIV is currently the most disguised virus. Notably, the HIV-1 virus has the highest rate of mutation, which helps in avoiding the immune system before evolving into forms that enable it to overcome the attacks initiated by the immune cells(6). Hence, it has degenerated into the world’s most prevalent cause of HIV infections.

The HIV-1 form of virus employs a shield cover that continues to shift the sugar molecules referred to as glycan. In this way, the antibodies are entirely prevented from attacking it. As a result, it continues to remain productive by devising survival means inside the human body. According to research by Ikanatha (3), HIV-1 has a protein cover called Env on its surface. Although this cover is supposed to be detected by the immune system, the virus can easily escape since the protein rapidly mutates, thus avoiding exposure.

More so, the ability to adapt rapidly is enhanced through the biological mechanism of the HIV-1 virus. It is made up of a singlestrand of RNA, which uses the reverse transcriptase enzyme in replicating the genome from various RNA bases of other viruses (7). The replication is quick and highly random, leading to the production of very many distinct copies. Here, it should be noted that recombination in a virus results in variation in genetic. Thus, tracing one unit of genetic combination, in this case, is almost impossible.

When replication is repeatedly done for a given period, it leads to the production of diverse pools of HIV copies referred to as quasi-species. Some of these species are incredibly functional and highly infectious (8). However, some are partly infectious. Other copies are merely junk and have no impact in contributing to infections (9). Besides, the immune system is designed such that it should respond to all species with varied sets of genetic combinations despite the level of infection (10). As such, therefore, the immune system is overworked and eventually becomes less effective.

Immune System is Impaired

The other reason why the virus is hard to kill is that once it enters the body, it attacks the helper T-Cells that eventually impairs the immune system. Notably, both adaptive and innate immune systems offer the body a natural defence mechanism against foreign objects and pathogens like allergens(11). Thus, it is difficult for the most viral infection to survive, such as a defence. However, HIV targets CD4 + T cells. They are among the cells that central to enhancing the performance of the immune system and ensuring the adaptability of the body(12). The reason is that the cells have the responsibility of coordinating other immune cell activities such as class switching of B cell antibodies, activation, and growth of cytotoxic cells as well as regulations of phagocytes bacterial activities (13). In this case, different immune cells are enabled to communicate constantly with other cells while coordinating the activities resulting in the formulation of overlapping networks against any infection(13). In most cases, the helper T-Cells are central in these network shields. They are involved in relying upon instructions across diverse sets of groups in the immune system to inform killer T-cells to destroy pathogens or activate B cells to produce antibodies (14). Since HIV develops within T-Cells, it grows to destruct and disrupt the coordinating process of the cell and the functioning of the shield network, thus forestalling the key immune processes.

Immune cells are left without an instructor. The impairment allows the HIV cells to replicate in a human body. Since significant cells such as B cells, other T Cells, and the innate immune system are left dormant without activators, the body becomes prone to attacks (15). Hence, one is exposed to cancer and opportunistic infections, as the immune system grows weak besidesan increase in the development of AIDS.

Conclusion

The review on the prevalence of HIV and AIDS in the United Kingdom indicates that there isa reduction in new infections as reported by declining diagnoses rate. However, different groups such as transgender people, men who have sex with other men, and heterosexual black African women and men are prone to infections. Besides, the discussion reveals that fighting HIV is almost impossible. The virus is highly mutative, which biologically gives it the ability to manoeuvre against destructive mechanisms of the body as initiated by the immune system. Besides, mutation yields a large number of unique genetic combinations that overworks the antibody system eventually rendering it ineffective.   The critical aspect of the survival of the virus is also exhibited in its target points of attack in the body. The virus attacks the central defence system of the body, which weakens the communication network thus hampering the functioning of other defence points. As a result, it gets the opportunity to replicate, further weakening the immune system. Although the war against HIV is hard, the UK has done the best to reduce the prevalence rate among its population. Hence, there is hope that the trend in declining infection will be sustained over time in the future.

Reference List

1. AVERT Charity. Global Information on HIV and AIDS: HIV and AIDS in the United Kingdom:https://www.avert.org/professionals/hiv-around-world/western-central-europe-north-america/uk
2. Herriott, N., Williams, C. & Ison, E.  Health Impact Assessment: evidence on health. Office for National Statistics, UK Publishers, 2010: https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/216006/dh_120109.pdf
3. Ikanatha, Nkuchia M. Infectious disease surveillance. Chichester: Wiley-Blackwell, 2013. Print.
4. Khot, Alex, and Andrew Polmear. Practical general practice: guidelines for effective clinical management. Edinburgh: Churchill Livingstone, 2010. Print.
5. Levene, L S., and Richard Donnelly. Management of type 2 diabetes mellitus: a practical guide. Edinburgh: Elsevier, 2008. Print.
6. Lucas, S. The Pathology of HIV Infections: https://www.lepra.org.uk/platforms/lepra/files/lr/Mar02/0009.pdf
7. Nattrass, Nicoli. The AIDS conspiracy: science fights back. New York: Columbia University Press, 2012. Print.
8. Rello, Jordi, and Kenneth Leeper. Severe community-acquired pneumonia. Boston: Kluwer Academic Publishers, 2001. Print.
9. Sabaté, Eduardo. Adherence to long-term therapies: evidence for action. Geneva: World Health Organization, 2003. Print.
10. Silvestri, Guido, and Mathias Lichterfeld. HIV-1 latency. Cham, Switzerland: Springer, 2018. Print.
11. Simon, V., Ho, D., Karim, A., Q. HIV/AIDS Epidemiology, Pathogenesis, Prevention, And Treatment: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2913538/
12. Tan, W. Y. Stochastic modeling of AIDS epidemiology and HIV pathogenesis. Singapore River Edge, N.J: World Scientific, 2000. Print.
13. Thomas, Felicity, Mary Knipe, and Peter Aggleton. Mobility, sexuality, and AIDS. London New York: Routledge, 2010. Print.
14. Webel, Allison R., et al. living a healthy life with HIV. Boulder, Colorado: Bull Publishing Company, 2016. Print.
15. World Health Organization. Managing epidemics: key facts about major deadly diseases. Geneva: World Health Organization, 2018. Print.