|Year : 2019 | Volume
| Issue : 2 | Page : 95-100
Coinfection between human immunodeficiency virus and tuberculosis: A consideration on ritonavir-related heme Oxygenase-1 pathway
Won Sriwijitalai1, Viroj Wiwanitkit2
1 TWS Medical Center, Bangkok, Thailand
2 Department of Biological Science, Joseph Ayobabalola University, Ikejo-Arakeji, Nigeria
|Date of Submission||07-Mar-2019|
|Date of Decision||05-May-2019|
|Date of Acceptance||10-May-2019|
|Date of Web Publication||17-Jun-2019|
Dr. Won Sriwijitalai
TWS Medical Center, Bangkok
Source of Support: None, Conflict of Interest: None
Background: Human immunodeficiency virus (HIV) infection is an important infection seen worldwide. HIV-infected patients usually have impaired immune function and get infected with other concurrent infections. Tuberculosis is a common concurrent infection in HIV-infected cases. The effect of coinfection and the response to the standard antiretroviral therapy in HIV-infected patients with concurrent tuberculosis infection is interesting. Methods: The aim of this study is to assess the effect of pharmacological pathway of ritonavir on tuberculosis treatment in HIV-infected patients with concurrent tuberculosis infection. The standard network pharmacology analysis is performed. Results: According to the network pharmacology analysis, the identified linkage is heme oxygenase-1. The ritonavir can result in increased expression of heme oxygenase-1 that further possible induces tuberculosis treatment failure in HIV-infected patients with concurrent tuberculosis infection. Conclusion: Ritonavir-related heme oxygenase-1 pathway is an important pathway that might affect the treatment of tuberculosis. Ritonavir dosage adjustment for tuberculosis treatment in HIV-infected patients with concurrent tuberculosis infection is necessary.
Keywords: Heme oxygenase-1, human immunodeficiency virus, ritonavir, tuberculosis
|How to cite this article:|
Sriwijitalai W, Wiwanitkit V. Coinfection between human immunodeficiency virus and tuberculosis: A consideration on ritonavir-related heme Oxygenase-1 pathway. Biomed Biotechnol Res J 2019;3:95-100
|How to cite this URL:|
Sriwijitalai W, Wiwanitkit V. Coinfection between human immunodeficiency virus and tuberculosis: A consideration on ritonavir-related heme Oxygenase-1 pathway. Biomed Biotechnol Res J [serial online] 2019 [cited 2022 Jan 29];3:95-100. Available from: https://www.bmbtrj.org/text.asp?2019/3/2/95/260482
| Introduction|| |
Immune system is an important system of human beings. This system is a specific defensive mechanism of the human body against foreign body.,,,,,,,,,,,, The immune system plays an important role for maintenance of normal physiological function and normal daily life. The disease of the immune system is also observable in clinical medicine, and this specific group of disease is called immune disease.,,,,,, The immune disease is a specific kind of medical problem that requires good clinical management. Some diseases might be congenital, whereas others are considered acquired problems.,,,,,, Since the immune system usually plays a role in disease defense, the disease of the immune system is usually difficult for management and becomes a big problem in clinical practice.
Human immunodeficiency virus (HIV) infection is an important infection seen worldwide. This infection is caused by a retrovirus which is known as HIV. This viral infection is the present problem in clinical medicine. Due to the direct lymphocyte attack of the virus, the infection can result in immunodeficiency problem.,,,,,,,,,,,,,,,,,, It is an important cause of acquired immunodeficiency disease. The infection has been detected for a few decades, but HIV infection becomes a very big public health problem of the world at present. Millions of HIV-infected patients are registered in several countries worldwide.
It is an important retrovirus infection that mainly affects the immune system of the patients and results in immunodeficiency. HIV can be transmitted through several modes including sexual contact, vertical transmission, and blood contact. Due to no curative therapy, HIV infection is still an important disease to be focused in global public health. Rutstein et al. noted that implementation of antiviral treatment into existing health systems is essential for prospective management of HIV infection. Rutstein et al. also noted that effective first-line regimens were very important.
HIV-infected patients usually have impaired immune function and get infected with other concurrent infections. A common coinfection in HIV-infected patients is tuberculosis. Tuberculosis is a common concurrent infection in HIV-infected cases. The effect of coinfection and the response to the standard antiretroviral therapy in HIV-infected patients with concurrent tuberculosis infection is interesting. Here, the authors focus interest on an important antiretroviral drug, ritonavir.
| Methods|| |
Aim of the study
The aim of this study is to assess the effect of pharmacological pathway of ritonavir on tuberculosis treatment in HIV-infected patients with concurrent tuberculosis infection. The standard network pharmacology analysis,, is performed. Basically, the standard network pharmacology is a novel approach in pharmacology. This new approach in pharmacology is based on the advanced concept of biochemioinformatics. As a biochemioinformatic approach, the network pharmacology approach is an approach based on informatic manipulation aiming at clarifying or predicting for a complete question, which is hereby in the specific field of pharmacology.,,,,,,,,,,,,, The approach is based on the concept of network analysis. Regarding network analysis, it is an informatic approach for grouping and rearranging of informatic data on pathways, which might be the cellular pathway or biochemical process. The mapping of the pathway data and searching for interrelationship for final construction of the web-linkage network for all included pathway data is the main process. This technique is accepted as a new useful for clinical pharmacology study. The technique was used in several previous international publications.,,,,,,,,
Based on the already mentioned of network pharmacology analysis, the present study was performed. First, the authors identified the pharmacological pathway of ritonavir. Then, the interrelationship with pathophysiological pathway of tuberculosis was done. All identified pathways were from direct literature searching for standard international databases (PubMed and Scopus). Briefly, the network mapping was done to represent the interrelationship. At first, the authors firstly performed data mining by searching on mentioned international databases. The focus of the search is to identify the information regarding pharmacological pathway of ritonavir and the pathophysiological pathway. From the search, the reports with complete available data were included for further informatic analysis. From all recruited publications derived from searching, the data on pathways were extracted for usage in further step in network pharmacology analysis. Regarding the next step, the derived pathways were identified and rearranged. Clarification on all included pathways was done to identify the possible common linkage among the pharmacological pathways of ritonavir and the pathophysiological pathways. The identification of common node at the linkage for common position between pharmacological pathways of ritonavir and the pathophysiological pathways was finally done. Then, the finalized new network representing the common pathway was constructed to represent identified final interrelationship between pharmacological pathways of ritonavir and the pathophysiological pathways and written in the final diagram format in the last step.
This study is a pure clinical pharmacoinformatic study that does not deal with human or animal subjects. It also does not involve a clinical specimen. Therefore, no written informed consent or ethical approval is required.
| Results|| |
According to the network pharmacology analysis, the main identified pathways for pharmacological reaction of ritonavir involve heme oxygenase-1, interleukin-8, tumor necrosis factor-alpha, chemokine ligand 5, and monocyte chemotactic protein 1., From interrelation analysis with tuberculosis, the identified linkage is heme oxygenase-1 [Figure 1]. The ritonavir can result in increased expression of heme oxygenase-1 that further possible induces tuberculosis treatment failure in HIV-infected patients with concurrent tuberculosis infection.
|Figure 1: Pharmacology network showing interrelationship between ritonavir pharmacological action and tuberculosis treatment|
Click here to view
| Discussion|| |
At present, there are many important viral infections in clinical medicine. HIV is one of the most important clinical problems in the present day. HIV infection is a big public health problem.,,,,,,,,,,,,,,,,,, It is still highly endemic in several countries worldwide. As noted by Paraskevis et al., HIV is responsible for one of the largest pandemic diseases in human history and it is still the present global problem. Despite a concerted global response for prevention and treatment, HIV infection is still the problem in many countries. HIV medicine research is required for the prevention of future transmission events. It is also a critical point for successful eliminating HIV. In the present day, HIV infection is still a big medical disease to be further studied. HIV medicine is an important issue in medicine that deals with HIV. The complex immunodeficiency status is the main clinical problem that has never been successfully managed until present. The diagnosis, treatment, and prevention of HIV are all the important issues in clinical medicine.
Due to the impairment of the immune system, there are several clinical problems due to the defect. Several diseases are seen in HIV-infected patients with defective immune status and those diseases are usually hard to manage. The possible diseases in HIV-infected patients might be diseases caused by several kinds of pathogens including bacteria, virus, fungus, and parasite.,,,,,,,,,,,,,, Furthermore, the abnormal immune system might result in uncontrolled tumorigenesis and cancer.,,, Regarding infectious diseases, both opportunistic and nonopportunistic infections are observable in HIV-infected cases. The linkage to the immunodeficiency status is usually mentioned in clinical literature. In routine clinical management of HIV-infected patients, the medical practitioner has to concern about the coinfection problem.,,,,,,,,,,,,,,,,,,,
A good example of coinfection seen in HIV-infected patients is the coinfection between HIV and tuberculosis. Basically, tuberculosis is a bacterial infection. The causative agent of tuberculosis is a mycobacterial pathogen, Mycobacterium tuberculosis. The tuberculosis is still an important public health problem globally. The infection can cause chronic lung infection. The patients with pulmonary tuberculosis might have some chronic pulmonary problems such as chronic cough and hemoptysis. The chronic fatigue and weight loss are also common clinical presentations in the patients infected with M. tuberculosis. At present, tuberculosis is still an important public health problem in several countries around the world, and there are numerous patients with tuberculosis. Tuberculosis can be seen in both immunocompromised and immunocompetent hosts. However, the problem usually exists in immunocompromised host such as HIV-infected patients.
The coinfection between HIV and tuberculosis is common.,,,,,,,,,, HIV infection and tuberculosis can affect the health of the patients. The concurrence of the two diseases might cause an increased clinical problem, and there might be additional pathology contributing as an effect of one another.,,, Regarding this concurrent infection problem, Tabarsi et al. studied the treatment outcome and mortality among HIV/tuberculosis-coinfected patients from Iran and concluded that the administration of antiretroviral therapy led to a better outcome. Indeed, antiretroviral therapy is the standard clinical management for HIV-infected patients.,,,,,,,, The antiretroviral therapy is aimed at the reduction of viral load that can be useful in control of immune impairment in the patients. It is usually difficult to manage these patients. Parallel treatment for both diseases is required, and the problem might be sometimes seen. Decloedt et al. recently studied the safety, effectiveness, and concentrations of adjusted lopinavir/ritonavir in HIV-infected adults on rifampicin-based antitubercular therapy and found that several factors including pregnancy, productive age group, gender, contraception, and comorbidity diseases were associated with treatment outcome. Mirsaeidi and Sadikot noted that host-specific factors play an important role in determining treatment outcome. Hence, it is necessary to have in-depth studies on the biological pathways involving in treatment process.
At present, there are several antiretroviral drugs that can be used in the management of HIV-infected patients. Ritonavir is a drug that is widely used at present. It is also proposed as an effective safe drug for the management of HIV-infected cases with concurrent tuberculosis. Amani-Bosse et al. noted that ritonavir antiretroviral therapy could result in effective virological response, but the important problem was adherence of HIV-infected patients to the antiretroviral drug use. Simpson et al. also showed the cost-effectiveness of using ritonavir antiretroviral therapy. Nevertheless, the important problem on the use of ritonavir in HIV-infected patients with tuberculosis is also observable. In the previous report, it can be observed that rifampin in tuberculosis treatment can alter the effectiveness of ritonavir antiviral therapy and it results in requirement for double dosing. In the present study, the network pharmacology analysis can show an opposite finding. It can show that the ritonavir treatment might also result in difficulty in tuberculosis treatment. According to the common pathway search, a common node at heme oxygenase-1 pathway can be observed.
The increased heme oxygenase-1 expression due to ritonavir use can further affect the tuberculosis treatment. Increased heme oxygenase-1 expression is related with tuberculosis treatment failure. On the other hand, the inhibition of heme oxygenase-1 expression results in suppression of the tuberculosis pathogen. The inhibition directly affects survival in human macrophage during pathogenic mycobacterial infection. As noted by Rockwood et al., M. tuberculosis induction of heme oxygenase-1 expression is dependent on oxidative stress. The heme oxygenase-1 expression is also accepted as a good biomarker for successful therapy in tuberculosis or HIV–tuberculosis infection. Indeed, the finding in the present study can confirm the statement proposed by Singh et al. that heme oxygenase-1 plays an important role in pathophysiology of several infections including HIV and tuberculosis.
This observation that ritonavir should be carefully used in the management of HIV-infected patients with concurrent tuberculosis infection. Adding to the already known inference effect of antituberculosis treatment on the effectiveness of antiretroviral therapy,,,,,,,,, the antiretroviral therapy can also affect the tuberculosis treatment on another side of the coin.
In case with HIV-infected patients with concurrent tuberculosis infection, the other antiretroviral drug rather than ritonavir might be more appropriate.
| Conclusion|| |
According to the present study, it reveals that ritonavir-related heme oxygenase-1 pathway is an important pathway that might counteract the effectiveness of tuberculosis treatment. This is a reason for requirement for adjustment for tuberculosis treatment in HIV-infected patients with concurrent tuberculosis infection.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Huse M. Mechanical forces in the immune system. Nat Rev Immunol 2017;17:679-90.
Parkin J, Cohen B. An overview of the immune system. Lancet 2001;357:1777-89.
Sforcin JM. Propolis and the immune system: A review. J Ethnopharmacol 2007;113:1-4.
Carrillo-Vico A, Guerrero JM, Lardone PJ, Reiter RJ. A review of the multiple actions of melatonin on the immune system. Endocrine 2005;27:189-200.
Alam R. A brief review of the immune system. Prim Care 1998;25:727-38.
Blalock JE, Smith EM. Conceptual development of the immune system as a sixth sense. Brain Behav Immun 2007;21:23-33.
Tomura M. Understanding of immune system by visualization of spatiotemporal regulation of immune cells in the entire body. Yakugaku Zasshi 2013;133:427-33.
Trakhtenberg EC. The effects of guided imagery on the immune system: A critical review. Int J Neurosci 2008;118:839-55.
Gallucci S, Matzinger P. Danger signals: SOS to the immune system. Curr Opin Immunol 2001;13:114-9.
Mahima, Ingle AM, Verma AK, Tiwari R, Karthik K, Chakraborty S, et al.
Immunomodulators in day to day life: A review. Pak J Biol Sci 2013;16:826-43.
Beilhack A, Rockson SG. Immune traffic: A functional overview. Lymphat Res Biol 2003;1:219-34.
McDade TW. Life history theory and the immune system: Steps toward a human ecological immunology. Am J Phys Anthropol 2003;Suppl 37:100-25.
Cooper EL. Comparative immunology. Curr Pharm Des 2003;9:119-31.
Baldovino S, Menegatti E, Roccatello D, Sciascia S. Immunological rare diseases. Adv Exp Med Biol 2017;1031:497-509.
Vanderlugt CL, Miller SD. Epitope spreading in immune-mediated diseases: Implications for immunotherapy. Nat Rev Immunol 2002;2:85-95.
Diaz-Gallo LM, Martin J. Common genes in autoimmune diseases: A link between immune-mediated diseases. Expert Rev Clin Immunol 2012;8:107-9.
Pereţianu D, Lotreanu V. A critical analysis of the current interpretation of immune diseases. Arguments for a more pathological classification. Med Interne 1989;27:149-62.
Shurin MR, Smolkin YS. Immune-mediated diseases: Where do we stand? Adv Exp Med Biol 2007;601:3-12.
Felsburg PJ. Overview of the immune system and immunodeficiency diseases. Vet Clin North Am Small Anim Pract 1994;24:629-53.
Mostarica-Stojković M. Mechanisms and classification of immunological diseases. Srp Arh Celok Lek 1994;122 Suppl 1:1-3.
Abraham GN, Khan AS. Human endogenous retroviruses and immune disease. Clin Immunol Immunopathol 1990;56:1-8.
Sabin CA, Lundgren JD. The natural history of HIV infection. Curr Opin HIV AIDS 2013;8:311-7.
Chu C, Pollock LC, Selwyn PA. HIV-associated complications: A systems-based approach. Am Fam Physician 2017;96:161-9.
Suthar AB, Granich RM, Kato M, Nsanzimana S, Montaner JS, Williams BG. Programmatic implications of acute and early HIV infection. J Infect Dis 2015;212:1351-60.
John M. The clinical implications of HIV infection and aging. Oral Dis 2016;22 Suppl 1:79-86.
Shenoy MK, Lynch SV. Role of the lung microbiome in HIV pathogenesis. Curr Opin HIV AIDS 2018;13:45-52.
Gardner EM, McLees MP, Steiner JF, Del Rio C, Burman WJ. The spectrum of engagement in HIV care and its relevance to test-and-treat strategies for prevention of HIV infection. Clin Infect Dis 2011;52:793-800.
Fauci AS, Pantaleo G, Stanley S, Weissman D. Immunopathogenic mechanisms of HIV infection. Ann Intern Med 1996;124:654-63.
Mirza A, Rathore MH. Pediatric HIV infection. Adv Pediatr 2012;59:9-26.
Davaro RE, Thirumalai A. Life-threatening complications of HIV infection. J Intensive Care Med 2007;22:73-81.
Stekler J, Collier AC. Primary HIV Infection. Curr HIV/AIDS Rep 2004 Jun; 1(2):68-73.
Knoll B, Lassmann B, Temesgen Z. Current status of HIV infection: A review for non-HIV-treating physicians. Int J Dermatol 2007;46:1219-28.
Apoola A, Ahmad S, Radcliffe K. Primary HIV infection. Int J STD AIDS 2002;13:71-8.
Marco CA, Rothman RE. HIV infection and complications in emergency medicine. Emerg Med Clin North Am 2008;26:367-87, viii-ix.
Chu C, Selwyn PA. Diagnosis and initial management of acute HIV infection. Am Fam Physician 2010;81:1239-44.
Cooper V, Clatworthy J, Harding R, Whetham J, Emerge Consortium. Measuring quality of life among people living with HIV: A systematic review of reviews. Health Qual Life Outcomes 2017;15:220.
Deeks SG, Overbaugh J, Phillips A, Buchbinder S. HIV infection. Nat Rev Dis Primers 2015;1:15035.
Robb ML, Ananworanich J. Lessons from acute HIV infection. Curr Opin HIV AIDS 2016;11:555-60.
Daniyal M, Akram M, Hamid A, Nawaz A, Usmanghani K, Ahmed S, et al.
Review: Comprehensive review on treatment of HIV. Pak J Pharm Sci 2016;29:1331-8.
Boulougoura A, Sereti I. HIV infection and immune activation: The role of coinfections. Curr Opin HIV AIDS 2016;11:191-200.
Rutstein SE, Ananworanich J, Fidler S, Johnson C, Sanders EJ, Sued O, et al.
Clinical and public health implications of acute and early HIV detection and treatment: A scoping review. J Int AIDS Soc 2017;20:21579.
Weld ED, Dooley KE. State-of-the-art review of HIV-TB coinfection in special populations. Clin Pharmacol Ther 2018;104:1098-109.
Mangum EM, Graham KK. Lopinavir-ritonavir: A new protease inhibitor. Pharmacotherapy 2001;21:1352-63.
Wang J, Li XJ. Network pharmacology and drug discovery. Sheng Li Ke Xue Jin Zhan 2011;42:241-5.
Boezio B, Audouze K, Ducrot P, Taboureau O. Network-based approaches in pharmacology. Mol Inform. 2017;36. doi: 10.1002/minf.201700048. [Epub ahead of print].
Berger SI, Iyengar R. Network analyses in systems pharmacology. Bioinformatics 2009;25:2466-72.
Li W, Yuan G, Pan Y, Wang C, Chen H. Network pharmacology studies on the bioactive compounds and action mechanisms of natural products for the treatment of diabetes mellitus: A review. Front Pharmacol 2017;8:74.
Yuan H, Ma Q, Cui H, Liu G, Zhao X, Li W, et al.
How can synergism of traditional medicines benefit from network pharmacology? Molecules 2017;22. pii: E1135.
Danhof M. Systems pharmacology – Towards the modeling of network interactions. Eur J Pharm Sci 2016;94:4-14.
Kibble M, Saarinen N, Tang J, Wennerberg K, Mäkelä S, Aittokallio T, et al.
Network pharmacology applications to map the unexplored target space and therapeutic potential of natural products. Nat Prod Rep 2015;32:1249-66.
Hao da C, Xiao PG. Network pharmacology: A Rosetta stone for traditional Chinese medicine. Drug Dev Res 2014;75:299-312.
Ye H, Wei J, Tang K, Feuers R, Hong H. Drug repositioning through network pharmacology. Curr Top Med Chem 2016;16:3646-56.
Azmi AS. Adopting network pharmacology for cancer drug discovery. Curr Drug Discov Technol 2013;10:95-105.
Chakraborty C, Doss C GP, Chen L, Zhu H. Evaluating protein-protein interaction (PPI) networks for diseases pathway, target discovery, and drug-design using 'in silico pharmacology'. Curr Protein Pept Sci 2014;15:561-71.
Wilson MR, Zoubeidi A. Clusterin as a therapeutic target. Expert Opin Ther Targets 2017;21:201-13.
Engin HB, Gursoy A, Nussinov R, Keskin O. Network-based strategies can help mono-and poly-pharmacology drug discovery: A systems biology view. Curr Pharm Des 2014;20:1201-7.
Zhao S, Iyengar R. Systems pharmacology: Network analysis to identify multiscale mechanisms of drug action. Annu Rev Pharmacol Toxicol 2012;52:505-21.
Jacunski A, Tatonetti NP. Connecting the dots: Applications of network medicine in pharmacology and disease. Clin Pharmacol Ther 2013;94:659-69.
Sandefur CI, Mincheva M, Schnell S. Network representations and methods for the analysis of chemical and biochemical pathways. Mol Biosyst 2013;9:2189-200.
Pérez-Nueno VI. Using quantitative systems pharmacology for novel drug discovery. Expert Opin Drug Discov 2015;10:1315-31.
Chandran U, Mehendale N, Tillu G, Patwardhan B. Network pharmacology of ayurveda formulation Triphala with special reference to anti-cancer property. Comb Chem High Throughput Screen 2015;18:846-54.
Chen L, Lv D, Wang D, Chen X, Zhu Z, Cao Y, et al.
Anovel strategy of profiling the mechanism of herbal medicines by combining network pharmacology with plasma concentration determination and affinity constant measurement. Mol Biosyst 2016;12:3347-56.
Wang Z, Wang YY. Modular pharmacology: Deciphering the interacting structural organization of the targeted networks. Drug Discov Today 2013;18:560-6.
Wu Z, Cheng F, Li J, Li W, Liu G, Tang Y. SDTNBI: An integrated network and chemoinformatics tool for systematic prediction of drug-target interactions and drug repositioning. Brief Bioinform 2017;18:333-47.
Huang J, Cheung F, Tan HY, Hong M, Wang N, Yang J, et al.
Identification of the active compounds and significant pathways of Yinchenhao decoction based on network pharmacology. Mol Med Rep 2017;16:4583-92.
Collier DA, Eastwood BJ, Malki K, Mokrab Y. Advances in the genetics of schizophrenia: Toward a network and pathway view for drug discovery. Ann N Y Acad Sci 2016;1366:61-75.
Cao Y, Lu X, Wang J, Zhang H, Liu Z, Xu S, et al.
Construction of an miRNA-regulated drug-pathway network reveals drug repurposing candidates for myasthenia gravis. Int J Mol Med 2017;39:268-78.
Greene CS, Voight BF. Pathway and network-based strategies to translate genetic discoveries into effective therapies. Hum Mol Genet 2016;25:R94-R98.
Li H, O'Donoghue AJ, van der Linden WA, Xie SC, Yoo E, Foe IT, et al.
Structure-and function-based design of plasmodium-selective proteasome inhibitors. Nature 2016;530:233-6.
Taylor N, Kremser I, Auer S, Hoermann G, Greil R, Haschke-Becher E, et al.
Hemeoxygenase-1 as a novel driver in ritonavir-induced insulin resistance in HIV-1-infected patients. J Acquir Immune Defic Syndr 2017;75:e13-e20.
Rockwood N, Costa DL, Amaral EP, Du Bruyn E, Kubler A, Gil-Santana L, et al. Mycobacterium tuberculosis
induction of heme oxygenase-1 expression is dependent on oxidative stress and reflects treatment outcomes. Front Immunol 2017;8:542.
Paraskevis D, Nikolopoulos GK, Magiorkinis G, Hodges-Mameletzis I, Hatzakis A. The application of HIV molecular epidemiology to public health. Infect Genet Evol 2016;46:159-68.
Manzardo C, Guardo AC, Letang E, Plana M, Gatell JM, Miro JM. Opportunistic infections and immune reconstitution inflammatory syndrome in HIV-1-infected adults in the combined antiretroviral therapy era: A comprehensive review. Expert Rev Anti Infect Ther 2015;13:751-67.
Tan IL, Smith BR, von Geldern G, Mateen FJ, McArthur JC. HIV-associated opportunistic infections of the CNS. Lancet Neurol 2012;11:605-17.
Gozhenko AI, Goydyk VS, Shukhtin VV, Goydyk NS, Servetskij SK. The dynamics of the incidence of opportunistic infections and somatic diseases HIV-infected patients who received inpatient treatment in 2006-2011. Lik Sprava 2015;1-2:9-17.
Miro JM, Agüero F, Duclos-Vallée JC, Mueller NJ, Grossi P, Moreno A, et al.
Infections in solid organ transplant HIV-infected patients. Clin Microbiol Infect 2014;20 Suppl 7:119-30.
Holmes CB, Losina E, Walensky RP, Yazdanpanah Y, Freedberg KA. Review of human immunodeficiency virus type 1-related opportunistic infections in Sub-Saharan Africa. Clin Infect Dis 2003;36:652-62.
Vergis EN, Mellors JW. Natural history of HIV-1 infection. Infect Dis Clin North Am 2000;14:809-25, v-vi.
Gallant JE, Moore RD, Chaisson RE. Prophylaxis for opportunistic infections in patients with HIV infection. Ann Intern Med 1994;120:932-44.
Rali P, Veer M, Gupta N, Singh AC, Bhanot N. Opportunistic pulmonary infections in immunocompromised hosts. Crit Care Nurs Q 2016;39:161-75.
Sedghizadeh PP, Mahabady S, Allen CM. Opportunistic oral infections. Dent Clin North Am 2017;61:389-400.
Dockrell DH, Edwards S, Fisher M, Williams I, Nelson M. Evolving controversies and challenges in the management of opportunistic infections in HIV-seropositive individuals. J Infect 2011;63:177-86.
El-Atrouni W, Berbari E, Temesgen Z. HIV-associated opportunistic infections. Bacterial infections. J Med Liban 2006;54:80-3.
Tsigrelis C, Berbari E, Temesgen Z. Viral opportunistic infections in HIV-infected adults. J Med Liban 2006;54:91-6.
Furrer H. Opportunistic diseases in HIV infection. Ther Umsch 2004;61:625-30.
Pasquet A, Yazdanpanah Y. HIV infection. Rev Prat 2012;62:255-62.
Rios A. HIV-related hematological malignancies: A concise review. Clin Lymphoma Myeloma Leuk 2014;14 Suppl: S96-103.
Manfredi R, Cascavilla A, Calza L. Non-AIDS-associated cancer disorders. A novel scenario after over thirty years from HIV discovery? Clinical experience and literature appraisal. Recenti Prog Med 2015;106:402-6.
Alvarnas JC, Zaia JA, Forman SJ. How I treat patients with HIV-related hematological malignancies using hematopoietic cell transplantation. Blood 2017;130:1976-84.
Aboulafia DM. Cancer screening in women living with HIV infection. Womens Health (Lond) 2017;13:68-79.
Lucas S, Nelson AM. HIV and the spectrum of human disease. J Pathol 2015;235:229-41.
Naidoo J, Mahomed N, Moodley H. A systemic review of tuberculosis with HIV coinfection in children. Pediatr Radiol 2017;47:1269-76.
Bruchfeld J, Correia-Neves M, Källenius G. Tuberculosis and HIV coinfection. Cold Spring Harb Perspect Med 2015;5:a017871.
Tavares AM, Fronteira I, Couto I, Machado D, Viveiros M, Abecasis AB, et al.
HIV and tuberculosis co-infection among migrants in Europe: A systematic review on the prevalence, incidence and mortality. PLoS One 2017;12:e0185526.
Tiberi S, Carvalho AC, Sulis G, Vaghela D, Rendon A, Mello FC, et al.
The cursed duet today: Tuberculosis and HIV-coinfection. Presse Med 2017;46:e23-39.
Tornheim JA, Dooley KE. Tuberculosis associated with HIV infection. Microbiol Spectr 20175. doi: 10.1128/microbiolspec.TNMI7-0028-2016. [Epub ahead of print].
Méndez-Samperio P. Diagnosis of tuberculosis in HIV co-infected individuals: Current status, challenges and opportunities for the future. Scand J Immunol 2017;86:76-82.
Lai RP, Meintjes G, Wilkinson RJ. HIV-1 tuberculosis-associated immune reconstitution inflammatory syndrome. Semin Immunopathol 2016;38:185-98.
Egelund EF, Dupree L, Huesgen E, Peloquin CA. The pharmacological challenges of treating tuberculosis and HIV coinfections. Expert Rev Clin Pharmacol 2017;10:213-23.
Lessells RJ, Swaminathan S, Godfrey-Faussett P. HIV treatment cascade in tuberculosis patients. Curr Opin HIV AIDS 2015;10:439-46.
Edge CL, King EJ, Dolan K, McKee M. Prisoners co-infected with tuberculosis and HIV: A systematic review. J Int AIDS Soc 2016;19:20960.
Dolan K, Wirtz AL, Moazen B, Ndeffo-Mbah M, Galvani A, Kinner SA, et al.
Global burden of HIV, viral hepatitis, and tuberculosis in prisoners and detainees. Lancet 2016;388:1089-102.
Scott L, da Silva P, Boehme CC, Stevens W, Gilpin CM. Diagnosis of opportunistic infections: HIV co-infections – Tuberculosis. Curr Opin HIV AIDS 2017;12:129-38.
Suarez GV, Vecchione MB, Angerami MT, Sued O, Bruttomesso AC, Bottasso OA, et al.
Immunoendocrine interactions during HIV-TB coinfection: Implications for the design of new adjuvant therapies. Biomed Res Int 2015;2015:461093.
Frasca K, Cohn J. Integration of HIV and tuberculosis in the community. J Int Assoc Provid AIDS Care 2014;13:534-8.
Tabarsi P, Chitsaz E, Moradi A, Baghaei P, Marjani M, Mansouri D. Treatment outcome and mortality: Their predictors among HIV/TB co-infected patients from Iran. Int J Mycobacteriol 2012;1:82-6. [Full text]
Palmisano L, Vella S. A brief history of antiretroviral therapy of HIV infection: Success and challenges. Ann Ist Super Sanita 2011;47:44-8.
Hamlyn E, Jones V, Porter K, Fidler S. Antiretroviral treatment of primary HIV infection to reduce onward transmission. Curr Opin HIV AIDS 2010;5:283-90.
Iyidogan P, Anderson KS. Current perspectives on HIV-1 antiretroviral drug resistance. Viruses 2014;6:4095-139.
Arts EJ, Hazuda DJ. HIV-1 antiretroviral drug therapy. Cold Spring Harb Perspect Med 2012;2:a007161.
Cihlar T, Fordyce M. Current status and prospects of HIV treatment. Curr Opin Virol 2016;18:50-6.
Pace M, Frater J. A cure for HIV: Is it in sight? Expert Rev Anti Infect Ther 2014;12:783-91.
Van den Eynde E, Podzamczer D. Switch strategies in antiretroviral therapy regimens. Expert Rev Anti Infect Ther 2014;12:1055-74.
Ambrosioni J, Nicolas D, Sued O, Agüero F, Manzardo C, Miro JM. Update on antiretroviral treatment during primary HIV infection. Expert Rev Anti Infect Ther 2014;12:793-807.
Deeks ED. Elvitegravir: A review of its use in adults with HIV-1 infection. Drugs 2014;74:687-97.
Mirsaeidi M, Sadikot RT. Patients at high risk of tuberculosis recurrence. Int J Mycobacteriol 2018;7:1-6.
] [Full text]
Azeez A, Ndege J, Mutambayi R. Associated factors with unsuccessful tuberculosis treatment outcomes among tuberculosis/HIV coinfected patients with drug-resistant tuberculosis. Int J Mycobacteriol 2018;7:347-54.
] [Full text]
Decloedt EH, Maartens G, Smith P, Merry C, Bango F, McIlleron H. The safety, effectiveness and concentrations of adjusted lopinavir/ritonavir in HIV-infected adults on rifampicin-based antitubercular therapy. PLoS One 2012;7:e32173.
Amani-Bosse C, Dahourou DL, Malateste K, Amorissani-Folquet M, Coulibaly M, Dattez S, et al.
Virological response and resistances over 12 months among HIV-infected children less than two years receiving first-line lopinavir/ritonavir-based antiretroviral therapy in Cote d'Ivoire and Burkina Faso: The MONOD ANRS 12206 cohort. J Int AIDS Soc 2017;20:21362.
Simpson KN, Baran RW, Kirbach SE, Dietz B. Economics of switching to second-line antiretroviral therapy with lopinavir/ritonavir in Africa: Estimates based on DART trial results and costs for Uganda and Kenya. Value Health 2011;14:1048-54.
Costa DL, Namasivayam S, Amaral EP, Arora K, Chao A, Mittereder LR, et al.
Pharmacological inhibition of host heme oxygenase-1 suppresses Mycobacterium tuberculosis
infection in vivo
by a mechanism dependent on T lymphocytes. MBio 2016;7. pii: e01675-16.
Scharn CR, Collins AC, Nair VR, Stamm CE, Marciano DK, Graviss EA, et al.
Heme oxygenase-1 regulates inflammation and mycobacterial survival in human macrophages during Mycobacterium tuberculosis
infection. J Immunol 2016;196:4641-9.
Andrade BB, Pavan Kumar N, Mayer-Barber KD, Barber DL, Sridhar R, Rekha VV, et al.
Plasma heme oxygenase-1 levels distinguish latent or successfully treated human tuberculosis from active disease. PLoS One 2013;8:e62618.
Singh N, Ahmad Z, Baid N, Kumar A. Host heme oxygenase-1: Friend or foe in tackling pathogens? IUBMB Life 2018;70:869-80.