How cigarette smoking affect human immunodeficiency virus (HIV) victims

Introduction

Cigarette smoking is a leading cause of morbidity and mortality in the general population (Lim et al., 2010) and it acts as a risk factor for many serious clinical conditions, including coronary artery disease, myocardial infection, stroke and pulmonary diseases. Moreover, in the general population smoking increases the risk for many types of cancers including cancers of the oral cavity, pharynx, esophagus, stomach, pancreas, lungs, cervix urinary bladder and kidney (Crothers et al., 2009).

The incidence of cigarette smoking is higher in HIV positive patients as compared to the general population. Many studies have reported rates over 40% (Lifson et al., 2010). This raises concern on a possible relationship between smoking and the increased rate of co-morbidities and death due to cardiovascular disease and cancer observed among HIV positive patients. In a research article by De (2009), he concluded that smoking influence the prevalence of pneumonia in HIV- positive patients and that cessation can reduce the risk by about 27%.

HIV positive cases tend to be more in people in the lower socioeconomic strata in which smoking is common and its adverse effects and to the burden of HIV infection and poverty. Several articles have suggested that smoking may modify CD4 lymphocyte counts but findings have not consistently established a relation between smoking and the course of HIV/AIDS (Wiewers et al., 2009).

The complication of respiratory tract of smoking including chronic obstructive pulmonary disease and respiratory infection which may include bacteria, tuberculosis and pneumonia. Smoking may also complicate several other disease conditions such as oral cavity cancers, pancreas cancer and kidney cancer etc.

HIV positive persons have been reported to have high instincts of smoking than the general public (Neuheus and Arriba, 2010). Many smoking related illnesses significantly affect HIV infected persons. Lung cancers and other malignancies have been seen as important causes of death among persons with HIV. As a result of the statements above, it is important to try to nullify the degree of disease or infection among HIV positive population that can be attributed to smoking.

Cigarette use is a worldwide phenomenon though smoking of cigarette is the most important prevalent form. Smoking is of utmost importance in public health worldwide and it is the largest single avoidable cause of all ill health and premature death in the general population (Robies and Ghin, 2008).

The health effects of cigarette smoking are many and are well known. The pattern of use in general population have been described in Nigeria (Ayankogbe et al., 2008). Since the advent of HIV in Nigeria in 1983, its subsequent pandemicity in many developing countries only little is known about its relationship with smoking.

Conceptual framework

Tobacco is an agricultural product from the fresh leaves of the plant in the genius Nicotiana. It is commercially available in dried, cured and natural forms. It is the basis of cigarette though it can be piped, dipped in between check, sniffed etc. The tobacco smoke contains nicotin and harinane which is a monoamine oxidase inhibitor. Both combine to give an addictive stimulant and euphoriant properties. Cigarette smoking is complex mixture of chemicals produced by burning tobacco and the additives. The smoke contains tar and its intake causes some fatal diseases such as lung cancer, bladder cancer (Routh et al., 2008).

Tobacco use kills about one-half of all life users. About 70 million people die yearly because of tobacco smoking. The increasing tobacco use may be because of strong tobacco marketing and lack of effective control by the government. In Nigeria, the prevalence of adult-smoking is about 8.6% (Shafey et al., 2008).

HIV in Nigeria

Human immunodeficiency virus (HIV) is an organism that causes acquired immune deficiency syndrome AIDS which results in the failure for the immune system thereby leading to the invasion of a life, opportunistic infection. As at 2012, Nigeria has HIV prevalence rate among adults of 15 – 49 years at 3.1% (Odutolu, 2006). Nigeria has the 2^nd largest number of people living with HIV (NACA, 2012). The HIV epidemic in Nigeria is complex and varies widely by region. In some states, the epidemic is more concentrated and it is driven by high-risk behaviours while in other states, it has more generalized epidemic that are sustained primarily by multiple sexual partnerships in the general population. Youth and young adults in Nigeria are particularly vulnerable to HIV with young women at higher risk than young men. There are several factors that may contribute to the spread of HIV, including  prostitution, high risk practices among itinerant workers, high prevalence of sexually transmitted infection (STI), elandestine high risk heterosexual and homosexual practices, international trafficking of women and irregular blood screening (Jedu-Agba et al., 2012).

The first two cases of HIV/AIDS in Nigeria were identified in 1985 and were reported at an international AIDS conference in 1986. And the Nigerian health sector established the National AIDS advisory committee which was shortly followed by the establishment of National Agency for the Control of Aids (NACA). In 1991, around 1.8% of the Nigerian populations were infected with HIV.

Despite increasing efforts to control the epidemic by 2006, it was estimated that just 10% of HIV infected women and men were receiving anti-retroviral therapy and only 70% of pregnant women were receiving treatment to reduce the risk of mother to child transmission of HIV (Clifford, Smith and Munoz, 2008). in 2010, a strategic frame work was launched whose aim includes: to reach 80% of sexually active adults and 80% of most at risk population with HIV counseling and testing; to ensure that 80% of eligible adults and 100% of eligible children are receiving ART, and to improve access to quality care and support services to at least 50% of people leaving with HIV (Vuyst et al., 2012)

Structure and genome of HIV

Human immuno-virus (HIV) is structurally different from other types of retro-viruses. It is almost spherical and has a diameter of 720nm and about 60 times smaller than a normal red blood cell. It has two copies of positive single stranded RNA that codes for the virus’s nine gene enclosed by a conical shaped capsid made up of 2000 copies of the viral protein p24. The Ribonucleic acid (RNA) is single stranded and tightly bound to necleo-capsid protein, p7, and the enzymes needed for the development of the virion. A matrix composed of the oral protein p17 surrounds the capsid ensuring the integrity of the virion particle (Castellsague and Diaz, 2006). This is also surrounded by the oral envelope which is made up of two layers of fatty molecules called phospholipids taken from the membrane of the human cell. Inside the viral envelopes are protein from the host cell and 70 copies of a complex HIV protein that protrudes through the surface of the virus particle and it is called glycoprotein 120. This glycoprotein complex enables the virus to attach to and fuse with target cells to initiate the infection cycle (Tiaun and Delancey, 2010).

The RNA genome is made up of seven structural landmarks (LRT, TAR, RRE, PE, SLIP, CRS and INS), nine genes (gag, pol, env, tat, rev, nef, vif, vpr and vpu). Pol, env and tat contain information needed to make the structural protein for new virus particles; thse six remaining genes are regulatory genes for protein that control the ability of hIV to infect cells, produce new copies and cause disease.

Classification of HIV

HIV is a member of the genius lentivirus (Ferlay, Shin and Bray, 2008), part of the family Retroviridae (Mbulaiteye and Bhatia, 2011). Lentivirus has many morphologies and biological properties in common. Many species are infected by lentiviruses which are characteristically responsible for living duration illnesses with a long period of incubation. They are transmitted as single stranded, positive sense enveloped RNA viruses. As soon as they enter into the target cell, the viral RNA genome is converted into a double stranded DNA by a virally encoded reverse transcriptase. The resultant viral DNA is then taken into the cell nucleus and integrated into the cellular DNA by a virally encoded integrase and host co-factor.

There are two types of HIV; HIV I and HIV II. HIV I is the virus that was initially discovered and termed both LAV and HTL III. It is more virulent and more infective and the cause of majority of HIV infection globally. The lower infectivity of HIV 2 compared to HIV I implies that the fewer of those exposed to HIV 2 will be infected per exposure. Because of its poor capacity for transmission HIV 2 is largely confined to West-Africa.

Replication cycle

1. Initial interaction between gp¹²⁰ and CD4⁺
2. Conformational change in gp¹²⁰ allows secondary interaction with Cek 5.
3. The distal tips of gp 41 are inserted into the cellular membrane
4. Gp41 undergoes significant conformational change: folding in half and forming coiled-coils. This process pulls the viral and cellular membranes together, fusing them. The HIV enters the macrophages and CD4+ cells by the absorption of glycoprotein on its surface to receptors on the target cell followed by fusion of the viral envelope with the cell membrane and the release of the HIV capsid into the cell.

The first step in fusion involves the high-affinity attachment  of the CD4 binding domains of gp120 to CD4, once this happens, the envelope complex undergoes a structural change, exposing the chemokine binding domains of gp120 and allowing them to interact with the target chemokine receptor. This allows for a more two pronged attachment which allows N-terminal fusion peptide gp4, to penetrate the cell membrane.

After HIV has bound to the target cell, the HIV, RNA and various enzymes including reverse transcriptiase, integrase, ribonuclease and protease are injected into the cell.

Assembly of new HIV I virions begins at the plasma membrane of the host cell. The polyprotein goes through the endoplasmic reticulum and it is transported to the Golgi-complex where it is cleaved by furin leading to HIV enveloping with glycoprotein. These are transported to the plasma membrane of the host cell where gp41 meets gp120.

Mode of transmission of HIV infection

Transmission of HIV occurs in several ways. Some include:

1. Having sexual intercourse with an infected partner
2. By injecting drugs using a needle or syringe which has already been used by someone who is infected
3. By blood transfusion of infected blood.

HIV can be passed on in these ways because the virus is present in the sexual fluids and blood of infected people. If infected blood or sexual fluid gets into your body, then you can become infected. But it depends on the type of body fluid. Saliva and sweat contain the HIV virus but not in sufficient quantities for transmission.

Vaginal sex: HIV is found in the sexual fluid of an infected person. For a man, this means in the fluid which comes out of the penis before and during sex. For a woman, it means HIV is in the fluids produced by the vagina before and during sex to help make intercourse easier. If a man with HIV has vaginal intercourse without protection, infected fluid can pass into the woman’s blood stream through a tiny cut or sore inside her body. Such a cut or sore wouldn’t always be visible and could be so small that the woman wouldn’t know about it. If a woman with HIV has sexual intercourse without protection, HIV could get into the man’s blood through a sore patch on his penis or by getting into the tube that runs down the penis.

If people have anal intercourse, the risk of infection doubles the vaginal intercourse because the lining of the anal is more delicate than those of the vagina, so it’s more likely to break during intercourse.

Injecting drugs: There is a good likelihood of becoming infected with HIV if you share hypodermic needles with someone who has the virus. The virus can be passed by sharing needles, syringes, spoons, filters and water. Disinfecting equipment between uses reduces the chance of transmission but does not eliminate it.

Blood transfusion: Some people have been infected through blood transfusion of infected blood. But these days all transfused blood are pre-tested before use. Except in cases of window period,, HIV transmission through blood transfusion is now rare. Other blood products such as packed cells, plasma and platelets are heat treated to make them safe.

Mother to child transmission: An infected pregnant woman can pass the virus on to her unborn baby either before or during birth. HIV can also be passed on during breast feeding.

Health care sector: Some health care workers have become infected with HIV by being stuck with needles, containing HIV infected blood. Only a few have had infection through open cuts or splashes into a mucous membrane.

Tattoos/piercing: Anything which allows another person’s body fluid to get inside your body is risky. If the equipment is not sterile, having a tattoo done could carry a small risk.

Signs and symptoms

The stages of HIV infection are acute, latency and AIDS infection. During the acute infection which lasts for several weeks, symptoms may includes: Fever, swollen lymph nodes, inflammation of the throat, rash, muscle pain, malaise, mouth and esophageal sores.

The latency state involves few or no symptoms and can last from two weeks to twenty years or more depending on the individual.

AIDS: The final stage of the infection is known by low CD4⁺ T cells, various opportunistic infections cancers and other conditions.

Epidemiology/prevalence

Worldwide Nigeria has the second highest number of new infections reported each year and estimates 3.4% of the populations are living with HIV. Although HIV prevalence is much lower in Nigeria than in the African countries, such as South Africa and Zambia, the size of Nigeria’s population means that in no distance future the number of people leaving with HIV will almost double. Approximately 210,000 people die yearly and the natural life expectancy is 56 years.

HIV prevalence is increasing worldwide because people on anti-retroviral therapy are living longer, although new infections decreased from 3.3 million to 2.3 million. Global AIDS related deaths peaked at 2.3 million before it decreased to 1.6 million by 2012. An estimated 9.7 million people in low income and middle-income countries had started anti-retroviral therapy. New insights into the mechanism of latent infection and the importance of reservoirs of infection might eventually lead to a cure. The role of immune activation is the pathogenesis of non-AIDS clinical events is receiving increased recognition. Breakthroughs in the prevention of HIV important to public health includes male medical circumcision, anti-retroviral to prevent mother to child transmission and anti-retroviral therapy in people with HIV to prevent transmission and anti-retroviral to pro-exposure prophylaxis.

In the study carried out by Kiral and Both (2008) prevalence of HIV ser-positive was 7.5% among smokers was obtained in the USA. in South Africa, the report of waweru and Anderson (2013) reported HIV positive among smokers to be 15%. In Nigeria, a prevalence of 3.4% was reported by Uzoma and Madibbo (2013), while in Rwanda, a prevalence of 24.3% was reported by (Leroy and Ladner, 2009), Kenya a prevalence of 26.7% was reported by (Memiah Agbor, 2012), In South Africa a prevalence of 66.3% was reported by (Moodley Hoofman), Uganda have a prevalence of 73% (Blossom, Beigi, 2007) and in Zambia a prevalence of 76.6% was obtained by (Parham and Hicks, 2006) respectively. In the various states of Nigeria, Ekiti has a prevalence of 10%, Benue has 10.6%, Delta has 2.1% and Kwara has 1.8% UNAIDS (2010). Another report by Akhigbe, Bamidela and Aodumin (2010) also reported Nigeria to have a prevalence of 5.3%.

HIV and cigarette smoking

The immunodeficiency produced by human immunodeficiency virus (HIV) infection predisposes the lung to both community acquired and opportunistic infections agents. The incidence of cigarette smoking among HIV infected individuals is notably higher than in the general population (Royce, 2009; Burns and Kramer, 2011). It has been shown that the incidence of bronchitis (Allen and Moore, 2006), bacterial pneumonia (Hirschtick and Jordan, 2005) and lung burden of HIV (Conley and Bush, 2006) is increased in HIV- positive smokers. These findings suggest that immune defects exist in HIV infected smokers. Yet, HIV negative smokers have significantly high percentages of CD4⁺ blood lymphocytes, than do non-smokers (Clarke and Taylor, 2008). Although park and colleagues (Park and Ferbas, 2012) and more recently Conley and coworkers, (Conley and Bush, 2006) have shown that upon sero-conversion, HIV infected smokers experience a marked decrease in CD4⁺ lymphocytes count, the decline only approaches the profiles of non-smokers at 2 years sero-conversion. This as assessed through blood CD4 cell counts, smoking does not appear to induce an immuno-comprised state.

In this regard, systemic immuno responses do not always reflect specific organ immunity. The compartment alised increase in CD4+ lymphocytes and increased CD4/CD13⁺ ratio seen in the lung but not in the blood of patient’s with sarcodosis is a case in point. Because blood CD4⁺ lymphocyte count reflect only systemic immune function, it may be necessary to examine organ immunologic indices separately. In the lungs of smokers, macrophages are immuno-suppressed for cell mediated immune responses. Smoker’s macrophages have a more inhibiting effect on lymphocytes proliferation than do non-smokers macrophages. Macrophages numbers are greatly increased by smoking (Niewochver, Rice, 2004),

From another perspective, smoker’s macrophages may also be impaired in the spontaneous release of cytokins (Brown and Iwanoto, 2009) Twigg (2004) have shown that smoking decreases lung macrophages in HIV infected individuals (Twigg 2004). This finding may be relevant to the understanding of certain HIV associated pulmonary complication since critical pro-inflammatory cytokins are important to lung defence against bacteria.

Laboratory diagnosis

HIV infection is identified either by the detection of HIV specific antibodies in serum or plasma or by demonstrating the presence of virus by nuclei acid detection using polymerase chain reaction (PCK), P24 antigen testing or rarely these days by growing the virus in cell culture. Antibody testing is the method most commonly used to diagnose HIV infection with the highly sensitive HIV I and HIV II enzyme immunoassay (EIA) tests currently on the market, sero conversion can detected within 2- 3 weeks of infection in majority of cases. In a small number of early sero-converters who are still in the window period, the p²⁴ antigen may below positive before antibody is detectable. Therefore, to enable the laboratory to select approximate testing, it is important to provide a clinical history that includes any relent high risk behaviour or symptoms consist with sero-conversion illness (CDC, 2011)

All HIV diagnostic laboratories should confirm repeatedly positive EIA screen tests with another assay. The Western blot most commonly used confirmatory test is a highly specific immunoblot that allows for the visualization of antibodies to the structural polypeptides of HIV. In cases where antibody testing may be insufficient to determine whether a patient is infected, it is necessary to perform a DNA PCR, a nuclei acid amplification method that allows for the detection of viral DNA integrated into the host cells genome. DNA PCR is very useful in testing infants of HIV. This is because infants may carry mother antibody for up to 15 months of age (Zhnag, Versadiove, 2012).

Prevention of HIV

To be able to prevent HIV infection, it is important to know the mode of transmission. This enables you to device means of prevention. There are six basic ways HIV spread can be prevented in any one population. These include

1. Do not have sex; Abstinence (Not having sex of any kind) is a sure way to avoid HIV infection through sexual contact.
2. Get tested and know your partner’s HIV status, talk to your partner about HIV testing and get tested before you have sex.
3. Be faithful to your partner. If you and your partner are both HIV negative and have sex only with each other, you are not at risk of HIV infection through sexual contact.
4. Use condoms: use a condom every time you have vaginal, anal or oral sex
5. Limit your number of sexual partners: if you have more than one sexual partner, get tested for HIV more regularly. Get tested and treated for sexually transmitted infections (STI) and insist that your partner do the same. Having an STI can increase your risk of becoming infected with HIV.
6. Don’t inject drugs: but if you do, use only clean needles and equipment and don’t share your equipment with others.

However, there are other ways of preventing HIV, some are;

1. Use of explosive prophylactics
2. Post exposure prophylactics
3. Prevention of mother to child transfusion of HIV

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