1. HIV latency and its translational implications
Introduction
Acquired immunodeficiency syndrome (AIDS) is a medical condition caused by human
immunodeficiency virus (HIV), and is characterized by significantly reduced plasma CD4 T cell
count (below 150/ml) and acquisition of rare cancers or/ and infections (e.g. Non-Hodgkin
lymphoma, tuberculosis, and candidiasis)[1]. 35 million people worldwide are infected by HIV,
vast majority of them are living in developing nations, especially in Sub-Saharan Africa. Of 35
million infected individuals, 3.2 are children[2].The introduction of antiretroviral therapy in
1986 was considered as a breakthrough in HIV infection/ AIDS as it reduced plasma viral load
significantly, prolonged the life expectation, and improved the quality of life of infected
people[3]. Unfortunately, incomplete virus eradication, drug resistance, side effects and high
cost put doubts on the future prospects of antiretroviral therapy in clinics[4]. Previous studies
revealed that reactivation of latent HIV in resting T cell is responsible for constant recurrence of
infection in patients who discontinued the therapy[5], putting urgent needs for new therapies.
Intriguingly, researchers proposed one so called “ shock and kill” strategy, which describes the
eradication of latent viral pool by inducing virus reactivation (hence “shock”) in complement
with antiretroviral therapy ( hence “kill”), giving hope for the development of new therapies.
However, one of the key questions needs to be elucidated is what causes HIV enters latency.
Tat, which has long been evident to be an viral transactivator that regulates initiation,
elongation processes, is crucial HIV latency biology [6,7]. Changes in cellular microenvironment,
viral gene transcription level and chromatin configuration are known factors that force HIV

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enters latent life cycle. What is noteworthy is that Tat does not work alone, requiring
cofactors(i.e. RTEFb, P-TEFB and NF-kB), which are potential drug targets.
This report is aimed at revising the recent advance in HIV infection/AIDS treatment. Firstly, HIV
latency biology and development of antiretroviral therapy will be introduced as foundations of
what led to the breakthrough and why we need the breakthrough in HIV/AIDS treatment.
Secondly, translational implications from research and other treatment alternatives will be
discussed. Finally, limitations of the breakthrough as well as other theories will be covered in
the discussion session.

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Early treatment-Antiretroviral therapies andtheir limitations
A. Development history
Antiretroviral therapies are combination of chemical drugs that suppress the entry,
replication and spread of HIV in cells. Combined antiretroviral therapies consist of several
inhibitors and are referred to as highly active anti-retroviral therapy (HAART)[8, WHO]. The
history of antiretroviral therapy originated from a clinical trial about zidovudine carried out
by Fischl and colleagues in 1986[9], since then Hammer et al proposed “triple-drug anti-HIV
therapy concept” based on the significant reduction of mortality rate in HIV infected who
were given indinavir-based HAARTs[10]. Antiretroviral therapies reduce plasma viral load,
improves CD4+T cell count (above 500 cells/ ul according to a report[11]) and the quality of
life. Nonetheless, treatment by antiretroviral therapy during the first decade is regretfully
unsuccessful[12]. The reasons for that will be discussed in the next session.
B. Limitations of antiretroviral therapies
A variety of antiretroviral drugs have been developed since its primary introduction. There
are five categories of antiretroviral drugs that are currently available: non-nucleoside
reverse transcriptase inhibitors (NNRTIs), nucleoside reverse transcriptase inhibitors
(NRTIs), protease inhibitors, entry and fusion inhibitors and integrase inhibitor[13]. Drugs of
each categories and their action mechanisms are listed below. Examples are given in
table1[14,15]. As effective and successful as antiretroviral drugs are meant to be,
observations of infection relapses, increased plasma viral load as well as reduced CD4+ T cell
count have been made in patients who discontinued their therapy. Moreover, considerable

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antiretroviral drugs that are currently being used in clinical practice have potential to cause
unwanted effects including nephrotoxicity, neurotoxicity, diarrhea, rash[16].
Table1. Examples of drugs of each categories
Table1: Names listed are the generic name of drugs. In clinical practice, different categories of
drugs are prescribed in combination to maximize the effectiveness of drugs.
Drug resistance, like in the drug treatment of any other infections caused by microorganisms,
especially in the treatment of bacterial infections, is inevitably identified in HIV infection/AIDS
treatment. The situation might be even worse regarding the fact that retrovirus, viral group to
which HIV belongs, has a very high mutation rate because of its single-stranded RNA genome,
which is not as stable as double-stranded DNA. Hence, it is strongly suggested that doctors
perform HIV genotypic resistance tests before prescribing the most appropriate and efficacious
antiretroviral drugs. Interestingly, there are debates about the availability of HIV genotypic
NNRTIs NRTIs Protease
inhibitor
Entry and fusion
inhibitor Integrase
inhibitor
Examples Festinavir,
Tenofovir
Nevirapine,
Efavirenz
Simeprevir,
Boceprevir
Albuvirtide Elitegravir

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resistance tests in areas where medical settings , putting constraints on wide-spread utilization
of genotypic testing[17]. Laethem et al suggest in their research that the next generation
sequencing technique has larger throughput and is more affordable[17]. Nevertheless, HIV
genotypic testing will not relive the drug resistance that the HIV infection/AIDS treatment
community currently suffer from. New hope relies in new therapeutic strategies.
Hints for new therapies-Understandings from HIV latency biology
A. Tat mediated transcriptional feedback loop
Tat was primary described by Sodroski and colleagues in 1985 as a viral transactivator that
regulates initiation, elongation processes of transcription[17]. Tat binds to viral DNA and recruits
transcription factors such as RTEFB and P-TEFB, for instance[18]. Hence, together they initiate
transcription of viral gene. Epigenetic modification of viral gene and viral gene transcription
interruption play crucial roles in HIV latency, although it is still controversial which one of them
is the primary cause[19,20]. Recent research shown Tat as potential causative agent of B cell
lymphoma in HIV infected individuals or AIDS patient[21], which might explain the prevalence of
B cell lymphoma in AIDS patients. That is important because studies of Tat in B cell lymphoma
will probably extend our knowledge about Tat biology in HIV latency.
B. Inducible reactivation from latency
HIV reservoir, resting CD4+ T cell, is the main obstacle for eradicating the virus by antiretroviral
therapies. Previous research carried out suggests induced virus reactivation in complement with
antiretroviral drug interventions as well as the immune systemof the host could facilitate virus
eradication [22]. Indeed, methyl transferase inhibitor and acetyl transferase inhibitors which
prevent epigenetic modification of viral genes, have been proven to be effective at inducing viral
reactivation[6].Furthermore, activation of T cell receptor (TCR) stimulated by alpha-CD3/CD28

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monoclonal antibodies causes reactivationof latent HIV by activating p-TEFb, which is anessential
transcription factor for HIV, and is usually suppressed by infected host cell as a defense
system.[11]. There are debates concerning inducible HIV reactivation could potentially cause
“HIV-associated complications”[23], but this worry is less significant when considering most of
the HIV infected individuals who received antiretroviral therapies are immune-competent.
Newlight-Translational implicationsfromHIVlatency biology research
Researche into HIV latency biology have led to one important outcome that is of greatest
translational implications. It is Tat-pTEFb interaction [29].
Transcription factor pTEFb comprises a cyclin-dependent kinase 9, CDK9[25] ,and a partner
cyclin T1, T2, or K[26]. Burlein and colleagues conducted an elegant study whereby they
designed a homogenous assay in Alpha LISA format using His-tagged pTEFb and biotinylated
Tat, which enabled the authors to observe the interaction between Tat and its cofactor
pTEFb[24]. Tat forms a quaternary complex with pTEFb and other molecules. Together, they
initiate the phosphorylation of viral RNA polymerase II and elongation of viral RNA[24]. Upon
infection, CD4+T cell initiates the conversion of pTEFb into RNP complex that comprises 7SK
RNA and 7SK RNP in resting T cells, resulting in dramatic decrease in intracellular pTEFb
level[25,26]. Therefore, HIV will not be able to replicate itself because of pTEFb deprivation.
Having said that, development of drugs that reverse the transformation of pTEFb into RNP
complexes or simply pTEFb transcription factor supply could induce reactivation of latent HIV.

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In addition, other therapeutic strategy such as HIV immunization is increasingly being revised as
potential new treatment. Immunization strategy includes therapeutic and preventive vaccine.
The former targets key molecules in HIV life cycle, preventing it from reactivation, replication,
and transmission to uninfected individuals[27]. Preventive vaccine, however, is dedicated to
preventing the virus from entering susceptible people[27]. Immunization strategies are more
cost-effective. This is of particular significance in under-developed area where antiretroviral
drugs are less available and affordable[38]. Examples of therapeutic and preventive vaccine
candidates (have not been proven to market) as well as their limitations and advantages are
listed in table2.
Table 2. The compare and contrast between therapeutic and preventive vaccines
Therapeutic vaccine Preventive vaccine
Examples Vacc-4x, Pep Tcell,
Thera Vax, Tat vaccine[34].
MRK rAd5, HVTN 502,
HVNT503, HVNT505[34].
Component Peptides, plasmid, viral
porteins, modified Tat.
HIV-1 Gag, Pol, Nef, and Env.
Advantages
Simple efficacy assessment,
facilitates the identification
of potential biomarkers that
can be drug targets, enhance
the effects of antiretroviral
drug[27].
Tat vaccine, which utilizes
biologically active viral Tat
protein to stimulate the body
to produce anti-Tat
antibodies, is considered as
the key to achieve anti-HIV
immunity[28,29]

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Limitations
Therapeutic vaccines are
effective only at the early
sate of HIV infection, which
contraindicates with the
current difficulties in making
early diagnosis[27].
Unlike therapeutic vaccines,
research into preventive
vaccine has been not fruitful
due to three reasons: 1) lack
of efficacy trial; 2) safety
concerns; 3) vaccines failed
to offer protection[30-34]
Table2. Vaccines listed are available at:
http://www.pipelinereport.org/sites/g/files/g575521/f/201407/Cure%20Immune%20Based
%20and%20Gene%20Therapies.pdf
Discussion
“Shock and kill” strategy is a new HIV/AIDS treatment characterized by induced reactivation of
latent HIV in combination with antiretroviral therapy. However, this proposal is in its infancy.
Considerable pharmaceutical and clinical trials are required to develop drugs that are capable
of inducing viral reactivation effectively and safely in patients.
Notably, there has been research suggesting virus eradication by preventing HIV reactivates
from latency. Szeto and colleagues demonstrated in their research that minocycline, an
immunomodulatory antibiotic, suppresses replication and reactivation of HIV. Hence has anti-
HIV effect[35]. Unlike conventional anti-HIV drugs which work by directly targeting HIV,
minocycline achieves its anti-HIV effect by altering cellular environment. More specifically,
minocycline causes dose-dependent decrease in viral RNA by downregulating the expression of
activation and proliferation biomarkers (e.g. CD25 and CCR5) in CD4+cell, and by decreasing cell

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cytokine (e.g. IFN-gamma and TNF-alpha) secretion level[36]. Mousseau et al also showed in
their publication that Didehydro-Cortistatin A (cDA) prevents HIV-1 from reactivating from
latency[37]. The authors proposed that dCA probably cause epigenetic changes in HIV viral
genome (no direct evidence showed there were epigenetic modification changes), concluding
from their observation of no viral reactivation even after withdrawal of dCA[37]. Those two
teams offered an opinion that is totally opposite to the rationale this report has been
discussing. This is interesting, especially when considering the advantages and disadvantages of
those two contrast strategies. Inducing viral reactivation is more robust, but has the potential
to cause HIV-associated complications in immuno-compromised patients. Preventing virus from
reactivating is soft, but it will inevitably cause “non-AIDS-associated disease” caused by
consistent release of provirus from infected CD4+T cell. In this regard, it is seems sensible to
seek more integrated treatment.
Amongst our limited choices, traditional Chinese medicine (TCM) is worth considering. As one
of the oldest medical systems ever been practiced by human-beings, TCM has invaluable clinical
utilization in terms of disease treatment in modern medicine system. As a matter of fact, TCM
has been proved to be effective at monitoring HIV/AIDS, cancer, and infertility[38-42]. Of
particular interest of this report, understanding of TCM in HIV/AIDS treatment will be discussed.
According to traditional Chinese medicine pattern identification, AIDS is defined as “yi bing”,
disease characterized by long latency, sudden onset, and serve symptoms[43], which is
interestingly consistent with the Western Medicine’s description of HIV/AIDS. Nevertheless,

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Western Medicine and TCMdo function in different systems and adapt inconsistent therapeutic
strategies and beliefs. For example, in the treatment of AIDS, TCM focuses on the treatment of
the patient with the disease rather than the disease to which western medicine pays
attention[43]. In addition, TCM is based on the utilization of herbs and other natural exist
material, which is completely different to the artificially synthesized chemicals used by Western
Medicine. Regretfully, despite of all those advantageous facts about TCM, it has yet not been
accepted and recommended by scientists and heath-care professionals word-wide[43]. This is
because there is a considerable lack of intensive clinical trails trying to elucidate the action
mechanisms of Chinese herbs[43]. In this regard, researchers proposed Complementary and
Integrate Medicine(CIM) based on the combination between TCMand Western Medicine,
which is a fast-developing area, and has been widely utilized in China for HIV/AIDS treatment.
Conclusion
Infection relapses, increase in plasma viral load , and decrease in CD4+ T cell count are observed
in HIV infected /AIDS patients when therapies are discontinued. This is probably because of the
conventional antiretroviral therapy’s failure to eradicate the virus from the patient’s body.
Unfortunately, the further employment of conventional antiretroviral drugs in clinical practice
is constrained by its limitations that are difficult to overcome. Encouragingly, a large number of
research has been conducted and proven to be fruitful, shedding light into the understandings
of HIV latency biology. Identification of Tat-mediated transcriptional feedback system,
particularly its cofactors, P-TEFB and NF-kB, is of great significance, giving translational
implications. Methyl transferase, acetyl transferase inhibitors, and anti-TCR monoclonal

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antibodies are receiving attention as viral reactivation inducers. New therapeutic strategies
such as preventive and therapeutic vaccines and CIM are the future HIV infection/AIDS
treatment development direction.

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Reference list:
1. (2015). Retrieved 9 August 2015, from http://www.aids.org/topics/hiv-resistance-testing/
2. Aids.gov,. (2015). Global Statistics. Retrieved 9 August 2015, from http://www.aids.gov/hiv-
aids-basics/hiv-aids-101/global-statistics
3. Hivinsite.ucsf.edu,. (2015). Opportunistic Infections and AIDS-Related Cancers. Retrieved 9
August 2015, from http://hivinsite.ucsf.edu/insite?page=pb-diag-04-00
4. Aids.gov,. (2015). Global Statistics. Retrieved 9 August 2015, from http://www.aids.gov/hiv-
aids-basics/hiv-aids-101/global-statistics
5. Finzi D, Hermankova M, Pierson T, Carruth LM, Buck C, Chaisson RE, et al. Identification of a
reservoir for HIV-1 in patients on highly active antiretroviral therapy. Science (80- ). 1997;278:
1295–300. doi:10.1126/science.278.5341.
6. Buchbinder SP, Mehrotra D V., Duerr A, Fitzgerald DW, Mogg R, Li D, et al. Efficacy
assessment of a cell-mediated immunity HIV-1 vaccine (the Step Study): a double-blind,
randomised, placebo-controlled, test-of-concept trial. Lancet. 2008;372: 1881–1893.
doi:10.1016/S0140-6736(08)61591-3
7. Barboric M, Peterlin BM. A new paradigm in eukaryotic biology: HIV Tat and the control of
transcriptional elongation. PLoS Biol. Public Library of Science; 2005;3: e76.
doi:10.1371/journal.pbio.0030076
8. Who.int,. (2015). WHO | Antiretroviral therapy. Retrieved 9 August 2015, from
http://www.who.int/topics/antiretroviral_therapy/en/
9. Fischl MA, Richman DD, Grieco MH, Gottlieb MS, Volberding PA, Laskin OL, et al. The efficacy
of azidothymidine (AZT) in the treatment of patients with AIDS and AIDS-related complex. A
double-blind, placebo-controlled trial. The New England journal of medicine. 1987.
doi:10.1056/NEJM198707233170401
10. Abacavir-lamivudine-zidovudine vs indinavir-lamivudine-zidovudine in antiretroviral-naive
HIV-infected adults: A randomized equivalence trial.(2001). Infectious Diseases In Clinical
Practice, 10(3), 171. doi:10.1097/00019048-200103000-00021
11. Geng, E., & Deeks, S. (2009). CD4 + T Cell Recovery with Antiretroviral Therapy: More Than
the Sum of the Parts. Clinical Infectious Diseases, 48(3), 362-364. doi:10.1086/595889
12.Hammer SM, Katzenstein DA, Hughes MD, Gundacker H, Schooley RT, Haubrich RH, et al. A
Trial Comparing Nucleoside Monotherapy with Combination Therapy in HIV-Infected Adults
with CD4 Cell Counts from 200 to 500 per Cubic Millimeter. New England Journal of Medicine.
1996. pp. 1081–1090. doi:10.1056/NEJM199610103351501
13. Warnke D, Barreto J, Temesgen Z. Antiretroviral drugs. J Clin Pharmacol. 2007;47: 1570–
1579. doi:10.1177/0091270007308034
14. De Clercq E. Antiretroviral drugs. Current Opinion in Pharmacology. 2010. pp. 507–515.

13. Pre-sessional Summer School Summative Report, 2015
Qilong Wu
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13
15. (2015). Retrieved 9 August 2015, from http://www.aids.org/topics/hiv-resistance-testing/
16. Fernandez-Montero J V, Eugenia E, Barreiro P, Labarga P, Soriano V. Antiretroviral drug-
related toxicities - clinical spectrum, prevention, and management. Expert Opin Drug Saf.
2013;12: 697–707. doi:10.1517/14740338.2013.806480
17. Van Laethem K, Theys K, Vandamme A-M. HIV-1 genotypic drug resistance testing: digging
deep, reaching wide? Curr Opin Virol. 2015;14: 16–23. doi:10.1016/j.coviro.2015.06.001
18. Nabel G, Baltimore D. An inducible transcription factor activates expression of human
immunodeficiency virus in T cells. Nature. 1987;326: 711–3. doi:10.1038/326711a0
19.Tyagi M, Pearson RJ, Karn J. Establishment of HIV latency in primary CD4+ cells is due to
epigenetic transcriptional silencing and P-TEFb restriction. J Virol. 2010;84: 6425–37.
doi:10.1128/JVI.01519-09
20. Duverger A, Jones J, May J, Bibollet-Ruche F, Wagner FA, Cron RQ, et al. Determinants of the
establishment of human immunodeficiency virus type 1 latency. J Virol. 2009;83: 3078–3093.
doi:10.1128/JVI.02058-08
21. Luzzi A, Morettini F, Gazaneo S, Mundo L, Onnis A, Mannucci S, et al. HIV-1 Tat induces
DNMT over-expression through microRNA dysregulation in HIV-related non Hodgkin
lymphomas. Infect Agent Cancer. 2014;9: 41. doi:10.1186/1750-9378-9-41
22. Ananworanich, J., & Mellors, J. (2015). A cure for HIV. Current Opinion In HIV And AIDS,
10(1), 1-3. doi:10.1097/coh.0000000000000125
23. Van der Plas, H., Meintjes, G., Schutz, C., Goliath, R., Myer, L., & Baatjie, D. et al. (2013).
Complications of Antiretroviral Therapy Initiation in Hospitalised Patients with HIV-Associated
Tuberculosis. Plos ONE, 8(2), e54145. doi:10.1371/journal.pone.0054145
24. Du Y, Khuri FR, Fu H. A homogenous luminescent proximity assay for 14-3-3 interactions
with both phosphorylated and nonphosphorylated client peptides. Curr Chem Genomics.
2008;2: 40–47. doi:10.2174/1875397300802010040
25. Price DH. P-TEFb, a Cyclin-Dependent Kinase Controlling Elongation by RNA Polymerase II.
Mol Cell Biol. 2000;20: 2629–2634. doi:10.1128/MCB.20.8.2629-2634.2000
26. Yik, J., Chen, R., Nishimura, R., Jennings, J., Link, A., & Zhou, Q. (2003). Inhibition of P-TEFb
(CDK9/Cyclin T) Kinase and RNA Polymerase II Transcription by the Coordinated Actions of
HEXIM1 and 7SK snRNA. Molecular Cell, 12(4), 971-982. doi:10.1016/s1097-2765(03)00388-5
27. Ensoli, B., Cafaro, A., Monini, P., Marcotullio, S., & Ensoli, F. (2014). Challenges in HIV
Vaccine Research for Treatment and Prevention. Front. Immunol., 5.
doi:10.3389/fimmu.2014.00417
28. Monini, P., Cafaro, A., Srivastava, I., Moretti, S., Sharma, V., & Andreini, C. et al. (2012). HIV-
1 Tat Promotes Integrin-Mediated HIV Transmission to Dendritic Cells by Binding Env Spikes and
Competes Neutralization by Anti-HIV Antibodies. Plos ONE, 7(11), e48781.
doi:10.1371/journal.pone.0048781

14. Pre-sessional Summer School Summative Report, 2015
Qilong Wu
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29. Bachler, B., Humbert, M., Palikuqi, B., Siddappa, N., Lakhashe, S., Rasmussen, R., &
Ruprecht, R. (2013). Novel Biopanning Strategy To Identify Epitopes Associated with Vaccine
Protection. Journal Of Virology, 87(8), 4403-4416. doi:10.1128/jvi.02888-12
30. Esparza, J. (2013). A brief history of the global effort to develop a preventive HIV vaccine.
Vaccine, 31(35), 3502-3518. doi:10.1016/j.vaccine.2013.05.018
31. Lema, D., Garcia, A., & De Sanctis, J. (2014). HIV Vaccines: A Brief Overview. Scand J
Immunol, 80(1), 1-11. doi:10.1111/sji.12184
32. Buchbinder, S., Mehrotra, D., Duerr, A., Fitzgerald, D., Mogg, R., & Li, D. et al. (2008).
Efficacy assessment of a cell-mediated immunity HIV-1 vaccine (the Step Study): a double-blind,
randomised, placebo-controlled, test-of-concept trial. The Lancet, 372(9653), 1881-1893.
doi:10.1016/s0140-6736(08)61591-3
33. Johnson, P., Schnepp, B., Zhang, J., Connell, M., Greene, S., & Yuste, E. et al. (2009). Vector-
mediated gene transfer engenders long-lived neutralizing activity and protection against SIV
infection in monkeys. Nature Medicine, 15(8), 901-906. doi:10.1038/nm.1967
34. Moorthy, V., Imoukhuede, E., Milligan, P., Bojang, K., Keating, S., & Kaye, P. et al. (2004). A
Randomised, Double-Blind, Controlled Vaccine Efficacy Trial of DNA/MVA ME-TRAP Against
Malaria Infection in Gambian Adults. Plos Med, 1(2), e33. doi:10.1371/journal.pmed.0010033
35. Szeto GL, Brice AK, Yang H-C, Barber SA, Siliciano RF, Clements JE. Minocycline attenuates
HIV infection and reactivation by suppressing cellular activation in human CD4+ T cells. J
Infect Dis. 2010;201: 1132–1140. doi:10.1086/651277
36. Dutta K, Basu A. Use of minocycline in viral infections. Indian Journal of Medical Research.
2011. pp. 467–470.
37.Szeto GL, Brice AK, Yang H-C, Barber SA, Siliciano RF, Clements JE. Minocycline attenuates
HIV infection and reactivation by suppressing cellular activation in human CD4+ T cells. J
Infect Dis. 2010;201: 1132–1140. doi:10.1086/651277
38.Dutta K, Basu A. Use of minocycline in viral infections. Indian Journal of Medical Research.
2011. pp. 467–470.
39.Huang S-T, Chen AP-C. Traditional Chinese medicine and infertility. Curr Opin Obstet
Gynecol. 2008;20: 211–215. doi:10.1097/GCO.0b013e3282f88e22
40.Ried K, Stuart K. Efficacy of Traditional Chinese Herbal Medicine in the management of
female infertility: A systematic review. Complementary Therapies in Medicine. 2011. pp.
319–331. doi:10.1016/j.ctim.2011.09.003
41.Cho WCS. Scientific evidence on the supportive cancer care with chinese medicine. Chinese
Journal of Lung Cancer. 2010. pp. 1 Anastasi JK, Chang M, Capili B, Dawes N.

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42.Traditional Chinese Medicine and Human Immunodeficiency Virus-Associated Neuropathy. J
Chinese Med. 2011; 16–20. 90–194. doi:10.3779/j.issn.1009-3419.2010.03.01
43. Chen W-T, Shiu C-S, Simoni J, Fredriksen-Goldsen K, Zhang F, Starks H, et al. Attitudes
toward antiretroviral therapy and complementary and alternative medicine in Chinese
patients infected with HIV. J Assoc Nurses AIDS Care. 2009;20: 203–17.
doi:10.1016/j.jana.2008.12.004