Annals of Clinical Cytology and Pathology

Human Papillomavirus at Multiple Sites Associated with Anal Squamous Intraepithelial Lesions in HIV-Seropositive Individuals

Research Article | Open Access

  • 1. Hawaii Center for AIDS, John A. Burns School of Medicine, University of Hawaii, USA
  • 2. Department of Tropical Medicine, Medical Microbiology & Pharmacology, John A. Burns School of Medicine, University of Hawaii, USA
  • 3. Office of Biostatistics and Quantitative Health Sciences, John A. Burns School of Medicine, University of Hawaii, USA
  • 4. John A. Burns School of Medicine, University of Hawaii Cancer Center, USA
  • 5. Department of Pathology, John A. Burns School of Medicine, University of Hawaii, USA
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Corresponding Authors
Bruce Shiramizu, Departments of Pediatrics, Medicine, & Tropical Medicine, University of Hawaii, Hawaii Center for AIDS, 651 Ilalo St. BSB 325AA, Honolulu, HI 96813, USA, Tel: 808-692-1677; Fax: 808-692-1984

Objective: HIV-Seropositive patients have higher risk of HPV infection even on anti-retroviral therapy. Infection with high-risk HPV genotypes can cause dysplasia leading to cancer. This study assessed HPV at different anatomical sites in HIV-seropositive individuals and factors associated with anal squamous intraepithelial lesions (ASIL).

Methods: Specimens were obtained from multiple anatomical sites for each participant in conjunction with routine screening for anal dysplasia. Female specimens included cervical and anal cytologies and oral wash. Male specimens included anal cytologies, oral wash, and exfoliated cells from penile head, penile shaft, scrotum, and from uncircumcised subjects, inner foreskin. Demographic and clinical characteristics were recorded. Following DNA extraction, HIV DNA copy was assessed by qPCR; HPV was genotyped. Statistical analyses included calculation of odds ratios (OR) and 95% confidence intervals (CI), t-tests or Mann-Whitney tests.

Results: Males were more likely to have ASIL: 29/50 (58%) compared to 1/11 females (9%) (OR=13.81, 95% CI: 1.64-116.32). HPV 6 or 11 in anal specimens was significantly associated with ASIL (OR= 6.29, 95% CI: 1.49-26.44). Number of HPV genotypes in anal specimens was also significant: ASIL+ (3.4 ± 3.1) versus ASIL- (1.6 ± 3.1) (p=0.009). Among 44 males, HPV was detected from at least one anatomical site for 33 participants (75%): 27 anus (61%), 19 oral wash (44%), 17 penile shaft (39%), 11 scrotum (26%), 10 penile head (23%), 0 foreskin. Detection of HPV in penile shaft specimens was significantly associated with ASIL (OR=6.79, 95% CI: 1.57-29.36) as was number of HPV genotypes in penile shaft specimens: ASIL+ (2.4 ± 4.0) versus ASIL- (0.6 ± 1.7) (p=0.025).

Only 1/11 females had ASIL; only 1/11 females had cervical dysplasia: OR was not estimable due to small numbers.

Conclusions: Males were more prone to ASIL than females. HPV at anal as well as non-anal sites may be indicative of ASIL.


Chuang E, Lim E, Milne C, Zhu X, Agsalda M, et al. (2016) Human Papillomavirus at Multiple Sites Associated with Anal Squamous Intraepithelial Lesions in HIV-Seropositive Individuals. Ann Clin Cytol Pathol 2(4): 1029.


•    Human papillomavirus
•    Anal cancer
•    Anal dysplasia
•    Human immunodeficiency virus
•    HPV
•    HIV


Individuals infected with human immunodeficiency virus type 1 (HIV) are at increased risk for human papillomavirus (HPV) infection and for anal dysplasia/cancer [1-4]. Presence of multiple HPV genotypes as well as presence of HPV at other anatomical sites potentially increase the risk for anal dysplasia/ cancer [1,2,5,6]. While high-risk HPV genotypes are found in more than 90% of anal cancers among HIV-infected patients, there may be additional factors that lead to anal dysplasia/cancer [6,7]. Coinfection with HIV and HPV in the anal canal and presence of HPV at other anatomical sites may support ongoing exposure to HPV and/or HIV-related immune suppression, leading to increased risk for dysplasia/cancer. Recent data suggest that the continued persistence of HIV DNA in circulating monocytes in patients treated with combination antiretroviral therapy (cART) leads to progression of HIV disease itself and other HIV-associated complications, which may include HPV infection and associated anal neoplasia [8-11]. The objective of this study was to evaluate specimens from various anatomical sites of the same HIV-positive individual for HPV genotypes in relation to anal squamous intraepithelial lesions (ASIL). We hypothesized that ASIL would be associated with presence of HPV at multiple anatomical sites.


During a 12-month period, men and women, 18–65 years of age, were either self-referred or referred by community physicians for anal dysplasia/cancer screening in collaboration with the Hawaii Center for AIDS, University of Hawaii (UH), and UH Cancer Center. Subjects were included if HIV-positive regardless of previous history of HPV infection, anal dysplasia/ cancer, or related treatment. Participants provided written consent in accordance with UH Institutional Review Board policy. Two anal cytology specimens were collected with a Dacron swab [12] and stored in ThinPrep collection medium (Hologic, Inc., Bedford, MA). One anal specimen was processed by a CLIA-certified clinical laboratory with cytopathology reviewed and reported by the same experienced cytopathologist (JK) according to the Bethesda system: anal cytology was evaluated, using criteria and terminology adapted from standardized cervical cytology screening [6,13-19]. The other anal specimen was assayed for HPV and HIV DNA. Anal cytology specimens were assessed for adequacy and categorized as 1) Negative (ASIL-) if no cellular changes could be detected or if cellular changes were caused by inflammation or reparative process or 2) Positive for anal squamous intraepithelial lesions (ASIL+) if abnormal cytological changes were found, including high-grade squamous intraepithelial lesions (HSIL), low-grade squamous intraepithelial lesions (LSIL), atypical squamous cells of undetermined significance (ASC-US), and atypical squamous cells which cannot exclude HSIL (ASC-H). Oral wash specimens were collected according to methods previously established [19]. From male participants, exfoliated cells from the penile glans/coronal sulcus, penile shaft, and scrotum were collected consecutively from each site and placed in separate collection vials as previously described [19]. Inner foreskin specimens were collected from uncircumcised subjects. Cervical cytology specimens were also obtained from female participants however no vaginal or vulva samplings were performed. Other data obtained per informed consent included plasma HIV RNA viral load and nadir CD4 cell count as well as age, gender, and ethnicity. Not all specimens and data were collected from all participants. DNA from each specimen was extracted using QIAamp DNA Micro Kit (Qiagen Inc, Valencia, CA) and analyzed for presence or absence of HPV DNA by PCR using a modified version of the PGMY09/PGMY11 primer system [20]. β-globin-positive and HPV DNA-positive specimens were genotyped using the Linear Array HPV Genotyping Test to detect 37 different HPV types (Roche Molecular Diagnostics, Pleasanton, CA), including 13 high-risk types (HPV 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68). Anal specimens had HIV DNA copy number quantified by real-time PCR as previously published [9]. Primers and probes included HIV gag (forward 5’-GAC ATC AAG CAG CCA TGC AA-3’; reverse 5’-CTC ATC TGG CCT GGT GCA AT-3’) and β−globin (forward 5’-AGG GCC TCA CCA CCA ACT TC; reverse 5’-TCA CTA GCA ACC TCA AAC AGA CAC C-3’) primers; and VIC-labeled HIV gag (5’ACC ATC AAT GAG GAA GCT GCA GAA TGG GA-3’) and FAM-labeled β-globin (5’-CTC CTG AGG AGA AGT CTG CCG TTA CTG CC-3’) probes. Controls included OM10.1 cells, each carrying a single, integrated HIV provirus; and water. Assays were performed in triplicate. Resulting data were analyzed using StepOne Plus software (Thermo Fisher Scientific, Waltham, MA). Copy numbers of each target gene were calculated based on the standard curve, and HIV DNA copy numbers per 1 x 106 cells were determined.

Statistical analyses were conducted by JABSOM Biostatistics & Quantitative Health Sciences. Mean age of participant subsets were compared using t-tests. Odds ratios (OR), 95% confidence intervals (CI), and p-values were calculated to investigate associations between anal cytology results (ASIL+ or ASIL-) and patient characteristics as well as HPV at various anatomical sites. For analyses, specimens were designated high-risk HPV-positive if one or more of 13 high-risk HPV genotypes (HPV 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68) was detected. The numbers of HPV genotypes or high-risk HPV genotypes per specimen were compared according to anal cytology results (ASIL+ or ASIL-) using Mann-Whitney tests. Kappa coefficient and McNemar’s test p-value were used to assess co-incident HPV genotypes.


Out of 61 participants (50 males and 11 females) enrolled in the study, 30 (49%) presented with ASIL. Data was not available to determine severity of atypical cytology. None of the participants were previously diagnosed with a relevant cancer. Mean age with standard deviation was similar for ASIL+ (50.1 ± 8.1) compared to ASIL- (47.4 ± 8.8) participants (p=0.275) as well as males (48.8 ± 9.1) compared to females (49.4 ± 5.2) (p=0.735) (Table 1). Men had significantly higher odds of presenting with ASIL: 29/50 (58%) compared to 1/11 (9%) women (OR=13.81, 95% CI: 1.64-116.32). Race/ethnicity was not a notable factor for ASIL: 13/27 (48%) non-White versus 17/34 (50%) White participants (OR=0.93, 95% CI: 0.38-2.55). All participants were HIV-seropositive and on combination antiretroviral therapy (cART), with 41/48 males (85%) and 9/9 females (100%) exhibiting undetectable plasma HIV levels. Data regarding length of HIV infection and cART use was not collected for this study. Participants with detectable viral levels had higher odds of presenting with ASIL though not statistically significant (OR=2.93, 95% CI: 0.52-16.58) (Table 1). Likewise, nadir CD4 ≤ 200 cells/mm3 conferred higher odds of ASIL but not statistically significant (OR=2.30, 95% CI: 0.80-6.61). Detectable HIV DNA in anal specimens was not associated with ASIL (OR=0.91, 95% CI: 0.31-2.64). Among 52 anal specimens collected and assayed, 29 (56%) were positive for any HPV; 20 (38%) were positive for one or more high-risk HPV genotypes (Figure 1). Genotypes detected most frequently in anal specimens included HPV 6 (17%) and 11 (15%), which are associated with genital warts; HPV 16 (19%), 52 (10%), and 68 (13%), which are high-risk types associated with cancer; as well as low-risk types like HPV 53 (12%), 55 (10%), 62 (17%), 66 (12%), 81 (13%), and 84 (12%). Other HPV genotypes were detected at frequencies below 10%. HPV in anal specimens conferred at least two-fold higher odds of ASIL (Table 2). Detection of HPV 6 or 11 in anal specimens was significantly associated with ASIL (OR=6.29, 95% CI: 1.49-26.44) while detection of any HPV approached statistical significance (OR=2.65, 95% CI: 0.86-8.24). The number of HPV genotypes detected in anal specimens was also significantly different for ASIL+ (3.4 ± 3.1) versus ASIL- (1.6 ± 3.1) participants (p=0.009). Multiple anatomical site specimens were collected from 44 males: 25 (57%) were ASIL+ while 19 (43%) were ASIL-. HPV was detected in these specimens as follows: 27/44 (61%) anal, 19/43 (44%) oral wash, 17/44 (39%) penile shaft, 11/43 (26%) scrotum, 10/44 (23%) penile head, and 0/7 foreskin. Overall, 33/44 (75%) males had at least one HPV+ specimen. HPV was detectable at more anatomical sites among ASIL+ (1.3 ± 1.8) versus ASIL- (0.6 ± 1.1) males (p=0.045). While 33/44 (75%) males were positive for any HPV across all anatomical sites, 25 (57%) were positive for one or more high-risk HPV genotypes (Figure 2). Across all specimens, genotypes detected most frequently among male participants included HPV 6 (30%) and 11 (18%), which are associated with genital warts; HPV 16 (25%), 18 (11%), 39 (16%), 45 (14%), 51 (11%), 52 (16%), 56 (16%), and 68 (20%), which are high-risk types associated with cancer; as well as low-risk types like HPV 53 (11%), 55 (18%), 61 (14%), 62 (30%), 66 (20%), 72 (14%), 81 (18%), 83 (11%) and 84 (25%). Other HPV genotypes were detected at frequencies below 10%. In relation to ASIL, the number of unique HPV genotypes detected across all anatomical sites per participant approached statistical significance: ASIL+ (5.3 ± 5.4) compared to ASIL- (2.6 ± 4.2) males (p=0.054). For all but one association between male specimen site and HPV variable tested, detectable HPV corresponded with increased odds of ASIL (Table 3). In particular, detection of HPV 16 or 18 proffered at least two-fold higher odds of ASIL across specimen types. Interestingly, penile shaft specimens displayed OR>3 across HPV variables. Any HPV in penile shaft specimens was significantly associated with ASIL (OR=6.79, 95% CI: 1.57-29.36) while detection of HPV 6 or 11 in anal specimens approached statistical significance (OR=4.19, 95% CI: 0.97-18.12). The number of HPV genotypes detected at some male specimen sites also differed according to ASIL status: significant for anal (p=0.0496) and penile shaft (p=0.025) specimens and approaching significance for scrotum (p=0.087) specimens (Table 4). Of 11 females enrolled in the study, only one presented with ASIL, and only one presented with cervical dysplasia. Odds ratios, 95% confidence intervals, and p-values were not estimable due to small numbers.

Table 1: Demographic and Clinical Characteristics of Participants and Association with ASIL.

  Anal Cytology, n      
Variable ASIL+ ASIL- OR 95% CI p-value
Age (yrs.), Mean ± SD 50.1 ± 8.1 47.7 ± 8.8     0.275
Gender (n=61)          
Male 29 21 13.81 1.64-116.32 0.016
Female 1 10      
Race/Ethnicity (n=61)          
White 17 17      
Asian 4 5      
Native Hawaiian 3 5      
Native American 3 2      
African-American 2 2      
Hispanic 1 0      
Nadir CD4 (n=58)*          
≤ 200 cells/mm3 19 12 2.30 0.80-6.61 0.121
> 200 cells/mm3 11 16      
Plasma HIV Viral Load (n=58)*          
Detectable 5 2 2.93 0.52-16.58 0.223
Not detectable 23 27      
Anal HIV DNA (n=59)*          
Detectable 10 11 0.91 0.31-2.64 0.861
Not detectable 19 19      
ASIL = anal squamous intraepithelial lesion
OR = odds ratio
95% CI = 95% confidence interval
SD = standard deviation
*Data not available for all participants

Table 2: Association between HPV in Anal Specimens (n=52) and ASIL.

  Anal Cytology, n      
Variable ASIL+ ASIL- OR 95% CI p-value
Any HPV          
Detectable 17 12 2.65 0.86-8.24 0.091
Not detectable 8 15      
Any high-risk HPV          
Detectable 12 8 2.19 0.70-6.85 0.177
Not detectable 13 19      
HPV 6 or 11          
Detectable 11 3 6.29 1.49-26.44 0.012
Not detectable 14 24      
HPV 16 or 18          
Detectable 7 4 2.24 0.57-8.84 0.251
Not detectable 18 23      
# HPV Genotypes, Mean ± SD 3.4 ± 3.1 1.6 ± 3.1     0.009
# High-risk HPV Genotypes, Mean ± SD 1.2 ± 1.5 0.5 ± 1.2     0.105
ASIL -Anal Squamous Intraepithelial Lesion
OR - Odds Ratio
95% CI = 95% confidence interval
SD - Standard Deviation



Among our participants, men presented with ASIL at a higher frequency than women. Male participants were predominantly men who have sex with men (MSM), whose behavioral factors place them at higher risk for anal dysplasia/cancer [21] though such risk factors were not assessed in this study. Consistent with literature, female participants presented with lower rates of anal and cervical dysplasia. ASIL did not differ by race/ ethnicity in our diverse group of participants. Previous studies have linked low CD4 cell counts to risk for ASIL. Bertisch et al. identified significant associations between anal cancer and low CD4 counts at nadir, at anal cancer diagnosis, and particularly 6-7 years before diagnosis [22]. While nadir CD4 and plasma HIV viral levels increased the odds of ASIL among our participants, the results were not statistically significant, perhaps owing to the small sample size. In the current cART era with effective reduction of HIV RNA to undetectable levels, presence of both HPV and residual HIV effects could establish a local, chronic inflammatory and metaplastic environment conducive to dysplastic expansion [9,23]. Contrary to expectations, detectable HIV DNA in anal specimens was not associated with ASIL. Analysis of HPV in anal specimens did produce some results consistent with current literature and knowledge. HIV-seropositive patients in our study exhibited a high frequency of HPV DNA present in anal specimens, with HPV 16 as the most frequently occurring genotype. Like previous studies, detectable anal HPV and the number of anal HPV genotypes was associated with ASIL [5]. Our results also showed a high degree of association between HPV 6 or 11 in anal specimens and ASIL. Further analysis demonstrated only slight agreement between anal specimens that were positive for HPV 6 or 11 and those positive for high-risk HPV (kappa=0.20, McNemar’s test p-value=0.11). Therefore, association between HPV 6 or 11 and ASIL is unlikely to be due to co-incidence of HPV 6 or 11 with high-risk HPV genotypes. Although HPV 6 and 11 are known for causing genital warts but not cancer, the pathologist’s finding of abnormal cellular changes may correspond to condyloma triggered by these genotypes. More surprising, however, were the associations between HPV in non-anal male specimens and ASIL. All but one association tested displayed higher odds of ASIL among males with HPV at non-anal sites. The association was particularly significant for detectable HPV in penile shaft specimens and less so for oral wash specimens; the variability among sites was corroborated by analysis of association between number of HPV genotypes at specimen site and ASIL. Although less well-studied, especially among HIV-positive MSM, penile HPV infection and penile intraepithelial neoplasia (PIN) have been recorded at lower rates than anal HPV infection and anal intraepithelial neoplasia (AIN) [24]. In a study of 263 HIVpositive MSM in Germany, Kreuter et al., reported 156 (59%) cases of AIN but only 11 (4%) of PIN [25]. Moreover, only 63% of penile cancers are attributable to HPV infection compared to 91% of anal cancers [26]. In light of this evidence, the high-degree of association between penile shaft HPV and ASIL in our study is unlikely to be due to co-incident penile dysplasia. Our discovery linking HPV at non-anal sites to ASIL may reflect autoinoculation -- transfer of HPV from the anus to other sites by the participant himself -- or behavioral factors among the predominantly MSM participants resulting in HPV introduction across multiple anatomical sites. Nevertheless, these results suggest that HPV at non-anal sites may also serve as indicators for ASIL among HIVpositive males. Previous studies of women have described strong concordance of HPV and dysplasia between cervical and anal sites as well as probable autoinoculation between the two [27- 29]. Only one HIV-positive female in our study presented with ASIL, and another presented with cervical dysplasia. Associations between cervical HPV and dysplasia with anal HPV and dysplasia could not be estimated due to small sample size. Few studies have reported on the clinical significance of HPV in non-anal sites with respect to ASIL risk in HIV-seropositive individuals. Rather, studies have reported on the natural history or presence of HPV in multiple genital sites irrespective of ASIL [6,7]. Our cross-sectional study reports for the first time that presence of HPV at multiple sites is associated with ASIL among HIV-positive males. Because HIV-seropositive individuals have an increased risk for anal dysplasia/cancer [1,3,30], studies that demonstrate HPV presence at non-anal sites may have important implications for diagnosis of anal dysplasia and for better understanding risk factors leading to anal cancer in the setting of HIV. Our study was limited by the number of participants enrolled after referral for routine anal dysplasia screening and by cross-sectional design. Future investigations warrant enrollment of larger numbers of patients to assess the relationship between ASIL and HPV at non-anal sites among men and women in the context of HIV.

Table 3: Association between HPV at Male Specimen Sites and ASIL.

  Specimen Site, OR (95% CI)
Variable Anus (n=44) Penile Head (n=44) Penile Shaft (n=44) Scrotum (n=43) Oral Wash (n=43)
Any HPV 1.91 (0.56-6.55) 4.00 (0.74-21.66) 6.79* (1.57-29.36) 2.67 (0.60-11.92) 1.71 (0.50-5.86)
Any high-risk HPV 1.58 (0.47-5.35) 3.43 (0.35-33.52) 3.31 (0.60-18.20) 2.57 (0.25-26.94) 1.78 (0.38-8.30)
HPV 6 or 11 4.19° (0.97-18.12) 0.75 (0.04-12.82) 5.68 (0.62-51.97) 1.64 (0.14-19.54) 1.64 (0.14-19.54)
HPV 16 or 18 2.07 (0.46-9.40) 4.15 (0.19-91.66) 3.43 (0.35-33.52) 6.35 (0.31-130.87) 4.33 (0.20-96.84)
ASIL-Anal Squamous Intraepithelial Lesion
OR-Odds Ratio
95% CI = 95% confidence interval
* Statistically significant (p=0.010)
° Approaching statistical significance (p=0.055)

Table 4: Association between Number of HPV Genotypes at Male Specimen Sites and ASIL.

  # HPV Genotypes, Mean ± SD
Specimen Site ASIL+ ASIL- p-value
Anus (n=44) 3.4 ± 3.1 1.9 ± 3.6 0.0496
Penile Head (n=44) 1.2 ± 2.9 0.5 ± 1.8 0.367
Penile Shaft (n=44) 2.4 ± 4.0 0.6 ± 1.7 0.025
Scrotum (n=43) 1.7 ± 3.6 0.5 ± 2.1 0.087
Oral Wash (n=43) 0.8 ± 1.3 0.5 ± 0.8 0.635
ASIL - Anal Squamous Intraepithelial Lesion
SD - Standard Deviation



The study was supported by grants U56CA096254, P20RR011091, U54CA143727, U01CA121947, U54RR026136, U54MD007584, G12MD007601, and P20GM103466 from the National Institutes of Health (NIH). The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH. A special thanks is extended to the participants of the study.

B.Y. Hernandez has received consultation fees from Merck, Inc. for work unrelated to this study.


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Received : 13 Jun 2016
Accepted : 10 Jul 2016
Published : 12 Jun 2016
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ISSN : 2573-1262
Launched : 2016
JSM Dental Surgery
ISSN : 2573-1548
Launched : 2016
Annals of Emergency Surgery
ISSN : 2573-1017
Launched : 2016
Annals of Mens Health and Wellness
ISSN : 2641-7707
Launched : 2017
Journal of Preventive Medicine and Health Care
ISSN : 2576-0084
Launched : 2018
Journal of Chronic Diseases and Management
ISSN : 2573-1300
Launched : 2016
Annals of Vaccines and Immunization
ISSN : 2378-9379
Launched : 2014
JSM Heart Surgery Cases and Images
ISSN : 2578-3157
Launched : 2016
Annals of Reproductive Medicine and Treatment
ISSN : 2573-1092
Launched : 2016
JSM Brain Science
ISSN : 2573-1289
Launched : 2016
JSM Biomarkers
ISSN : 2578-3815
Launched : 2014
JSM Biology
ISSN : 2475-9392
Launched : 2016
Archives of Stem Cell and Research
ISSN : 2578-3580
Launched : 2014
Annals of Clinical and Medical Microbiology
ISSN : 2578-3629
Launched : 2014
JSM Pediatric Surgery
ISSN : 2578-3149
Launched : 2017
Journal of Memory Disorder and Rehabilitation
ISSN : 2578-319X
Launched : 2016
JSM Tropical Medicine and Research
ISSN : 2578-3165
Launched : 2016
JSM Head and Face Medicine
ISSN : 2578-3793
Launched : 2016
JSM Cardiothoracic Surgery
ISSN : 2573-1297
Launched : 2016
JSM Bone and Joint Diseases
ISSN : 2578-3351
Launched : 2017
JSM Bioavailability and Bioequivalence
ISSN : 2641-7812
Launched : 2017
JSM Atherosclerosis
ISSN : 2573-1270
Launched : 2016
Journal of Genitourinary Disorders
ISSN : 2641-7790
Launched : 2017
Journal of Fractures and Sprains
ISSN : 2578-3831
Launched : 2016
Journal of Autism and Epilepsy
ISSN : 2641-7774
Launched : 2016
Annals of Marine Biology and Research
ISSN : 2573-105X
Launched : 2014
JSM Health Education & Primary Health Care
ISSN : 2578-3777
Launched : 2016
JSM Communication Disorders
ISSN : 2578-3807
Launched : 2016
Annals of Musculoskeletal Disorders
ISSN : 2578-3599
Launched : 2016
Annals of Virology and Research
ISSN : 2573-1122
Launched : 2014
JSM Renal Medicine
ISSN : 2573-1637
Launched : 2016
Journal of Muscle Health
ISSN : 2578-3823
Launched : 2016
JSM Genetics and Genomics
ISSN : 2334-1823
Launched : 2013
JSM Anxiety and Depression
ISSN : 2475-9139
Launched : 2016
Clinical Journal of Heart Diseases
ISSN : 2641-7766
Launched : 2016
Annals of Medicinal Chemistry and Research
ISSN : 2378-9336
Launched : 2014
JSM Pain and Management
ISSN : 2578-3378
Launched : 2016
JSM Women's Health
ISSN : 2578-3696
Launched : 2016
Clinical Research in HIV or AIDS
ISSN : 2374-0094
Launched : 2013
Journal of Endocrinology, Diabetes and Obesity
ISSN : 2333-6692
Launched : 2013
Journal of Substance Abuse and Alcoholism
ISSN : 2373-9363
Launched : 2013
JSM Neurosurgery and Spine
ISSN : 2373-9479
Launched : 2013
Journal of Liver and Clinical Research
ISSN : 2379-0830
Launched : 2014
Journal of Drug Design and Research
ISSN : 2379-089X
Launched : 2014
JSM Clinical Oncology and Research
ISSN : 2373-938X
Launched : 2013
JSM Bioinformatics, Genomics and Proteomics
ISSN : 2576-1102
Launched : 2014
JSM Chemistry
ISSN : 2334-1831
Launched : 2013
Journal of Trauma and Care
ISSN : 2573-1246
Launched : 2014
JSM Surgical Oncology and Research
ISSN : 2578-3688
Launched : 2016
Annals of Food Processing and Preservation
ISSN : 2573-1033
Launched : 2016
Journal of Radiology and Radiation Therapy
ISSN : 2333-7095
Launched : 2013
JSM Physical Medicine and Rehabilitation
ISSN : 2578-3572
Launched : 2016
Annals of Clinical Pathology
ISSN : 2373-9282
Launched : 2013
Annals of Cardiovascular Diseases
ISSN : 2641-7731
Launched : 2016
Journal of Behavior
ISSN : 2576-0076
Launched : 2016
Annals of Clinical and Experimental Metabolism
ISSN : 2572-2492
Launched : 2016
Clinical Research in Infectious Diseases
ISSN : 2379-0636
Launched : 2013
JSM Microbiology
ISSN : 2333-6455
Launched : 2013
Journal of Urology and Research
ISSN : 2379-951X
Launched : 2014
Journal of Family Medicine and Community Health
ISSN : 2379-0547
Launched : 2013
Annals of Pregnancy and Care
ISSN : 2578-336X
Launched : 2017
JSM Cell and Developmental Biology
ISSN : 2379-061X
Launched : 2013
Annals of Aquaculture and Research
ISSN : 2379-0881
Launched : 2014
Clinical Research in Pulmonology
ISSN : 2333-6625
Launched : 2013
Journal of Immunology and Clinical Research
ISSN : 2333-6714
Launched : 2013
Annals of Forensic Research and Analysis
ISSN : 2378-9476
Launched : 2014
JSM Biochemistry and Molecular Biology
ISSN : 2333-7109
Launched : 2013
Annals of Breast Cancer Research
ISSN : 2641-7685
Launched : 2016
Annals of Gerontology and Geriatric Research
ISSN : 2378-9409
Launched : 2014
Journal of Sleep Medicine and Disorders
ISSN : 2379-0822
Launched : 2014
JSM Burns and Trauma
ISSN : 2475-9406
Launched : 2016
Chemical Engineering and Process Techniques
ISSN : 2333-6633
Launched : 2013
JSM Allergy and Asthma
ISSN : 2573-1254
Launched : 2016
Journal of Neurological Disorders and Stroke
ISSN : 2334-2307
Launched : 2013
Annals of Sports Medicine and Research
ISSN : 2379-0571
Launched : 2014
JSM Sexual Medicine
ISSN : 2578-3718
Launched : 2016
Annals of Vascular Medicine and Research
ISSN : 2378-9344
Launched : 2014
JSM Biotechnology and Biomedical Engineering
ISSN : 2333-7117
Launched : 2013
Journal of Hematology and Transfusion
ISSN : 2333-6684
Launched : 2013
JSM Environmental Science and Ecology
ISSN : 2333-7141
Launched : 2013
Journal of Cardiology and Clinical Research
ISSN : 2333-6676
Launched : 2013
JSM Nanotechnology and Nanomedicine
ISSN : 2334-1815
Launched : 2013
Journal of Ear, Nose and Throat Disorders
ISSN : 2475-9473
Launched : 2016
JSM Ophthalmology
ISSN : 2333-6447
Launched : 2013
Journal of Pharmacology and Clinical Toxicology
ISSN : 2333-7079
Launched : 2013
Annals of Psychiatry and Mental Health
ISSN : 2374-0124
Launched : 2013
Medical Journal of Obstetrics and Gynecology
ISSN : 2333-6439
Launched : 2013
Annals of Pediatrics and Child Health
ISSN : 2373-9312
Launched : 2013
JSM Clinical Pharmaceutics
ISSN : 2379-9498
Launched : 2014
JSM Foot and Ankle
ISSN : 2475-9112
Launched : 2016
JSM Alzheimer's Disease and Related Dementia
ISSN : 2378-9565
Launched : 2014
Journal of Addiction Medicine and Therapy
ISSN : 2333-665X
Launched : 2013
Journal of Veterinary Medicine and Research
ISSN : 2378-931X
Launched : 2013
Annals of Public Health and Research
ISSN : 2378-9328
Launched : 2014
Annals of Orthopedics and Rheumatology
ISSN : 2373-9290
Launched : 2013
Journal of Clinical Nephrology and Research
ISSN : 2379-0652
Launched : 2014
Annals of Community Medicine and Practice
ISSN : 2475-9465
Launched : 2014
Annals of Biometrics and Biostatistics
ISSN : 2374-0116
Launched : 2013
JSM Clinical Case Reports
ISSN : 2373-9819
Launched : 2013
Journal of Cancer Biology and Research
ISSN : 2373-9436
Launched : 2013
Journal of Surgery and Transplantation Science
ISSN : 2379-0911
Launched : 2013
Journal of Dermatology and Clinical Research
ISSN : 2373-9371
Launched : 2013
JSM Gastroenterology and Hepatology
ISSN : 2373-9487
Launched : 2013
Annals of Nursing and Practice
ISSN : 2379-9501
Launched : 2014
JSM Dentistry
ISSN : 2333-7133
Launched : 2013
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