HPV infection and its correlation with p53 and Bcl-2 among pregnant mothers and their infants.

The investigation of perinatal transmission of HPV is vital for early screening of cervical/oral cancers. Here, transmission of HPV from the pregnant women to their infants was studied. p53 and Bcl-2 expressions and their correlations with HPV infection were examined. HPV infection was detected in the cervical and oral swabs of 135 mother-baby pairs employing both PCR and HC-II methods. 1 year follow-up with an interim visit at 3 months for mothers and 6 months for babies was performed. Immunocytochemistry of p53 and Bcl-2 using the streptavidin-biotin peroxidase method was performed. Prevalence of HPV infection in the mothers was 28.14%, (38/135) and 30.37% (41/135) determined by the PCR and HC-II methods respectively. HPV 16 and/or 18 was identified in 81.57% (31/38) and 82.92% (34/41) of the HPV + women estimated by PCR and HC-II methods respectively. Prevalence rate of HPV 16 among the HPV + pregnant women was 63.15% (24/38) and 65.85% (27/41) determined by PCR and HC-II methods respectively. The frequency of perinatal transmission was 21.05% (8/38) and 21.95% (9/41) determined by PCR and HC-II methods respectively at birth. The HPV + infants in the follow up study cleared the infection within 6 weeks. An abnormal nuclear expression of p53 and cytoplasmic expression of Bcl-2 were observed in the HPV + mother-baby pairs. Cesarean section did not protect the infants against perinatal HPV transmission. The detection of p53 and Bcl-2 proteins in the HPV + mother-baby pairs suggests that these biomarkers may be important in the early screening of oral/cervix cancers in positive cases.

Liposome-encapsulated glycyrrhizin alleviates hyperglycemia and glycation-induced iron-catalyzed oxidative reactions in streptozotocin-induced diabetic rats.

Glycyrrhizin, a bioactive constituent of Glycyrrhiza glabra has been reported to ameliorate diabetes. Here, the effects of liposome-encapsulated glycyrrhizin on STZ-induced diabetes and associated oxidative stress were investigated. Wistar rats were grouped as control (NC, received placebo), diabetic (DC, STZ-induced), diabetic treated with free glycyrrhizin (DTG, 3 i.v. doses, 1.6 mg/0.5 ml), empty liposomes (DTl, 3 i.v. doses), and liposome-encapsulated glycyrrhizin (DTbd, 3 i.v. doses, 1.6 mg/0.5 ml). Serum glucose, insulin, intraperitoneal glucose tolerance test and glycohemoglobin were estimated. Free iron and iron-mediated oxidative stress were examined. Histological examinations of the kidney and liver were performed. Liposomal-glycyrrhizin treatment caused significant improvement of hyperglycemia (DC vs. DTbd p < .05), glucose intolerance (DC vs. DTG p < .01 and DC vs. DTbd p < .05), insulin (DC vs. DTG p < .1, DTbd vs. DC p < .05 and DTbd vs. DTG p < .1) and glycohemoglobin (DC vs. DTG p < .1 and DC vs. DTbd p < .05) levels in the DTbd group. Alleviation of free iron release (DC vs. DTbd p < .05), lipid peroxidation (DC + H2O2 vs. DTbd + H2O2 p < .05), deoxyribose (DC + H2O2 vs. DTbd + H2O2, p < .05), and DNA degradation occurred in the DTbd group. The abnormalities of the kidney and liver were abolished in the DTbd group. The inhibitory effects were more pronounced compared to free glycyrrhizin. Liposome-encapsulated glycyrrhizin treatment caused inhibition of diabetic complications through its antioxidant effects and can be exploited for effective treatment of diabetes.

Glycyrrhiza glabra alcoholic root extract ameliorates hyperglycemia, hyperlipidemia, and glycation-induced free iron-mediated oxidative reactions.

Hyperglycemia-associated oxidative stress leads to various pathophysiological complications in diabetes mellitus. Here, the effects of Glycyrrhiza glabra (G. glabra) root extract of streptozotocin (STZ)-induced diabetic changes and the associated free iron-mediated oxidative reactions were investigated. The animals were divided into five group, Group 1: Control (NC received buffer); Group 2: STZ-induced (DC); Group 3: Control treated with G. glabra root extract (NT, 60 mg/Kg b.w daily for 1 month); Group 4: Diabetic treated with the extract (60 mg/Kg b.w daily for 1 month); Group 5: Diabetic treated with glibenclamide (DTG, 8.6 mg/Kg b.w for 1 month). STZ (i) induced hyperglycemia, abnormal intraperitoneal glucose tolerance test (IPGTT), increased HbA1c and decreased plasma insulin levels (ii) hyperlipidemia (iii) lowered antioxidant enzyme activities (iv) diminished RBC membrane fluidity (v) enhanced hemoglobin glycation-induced iron release and associated free radical reactions. Treatment with the extract resulted in significant reversal of hyperglycemia (DC: 205.0 ± 7.0 mg/dl vs. DT: 87.5 ± 4.5 mg/dl, p < .05); HbA1c (DC: 11.5 ± 2.0 vs. DT: 7.5 ± 0.8 vs. DT: 7.5 ± 0.8, p < .05); insulin (DC: 0.3 ± 0.06 vs. DT: 1.25 ± 0.15 µgm/L, p < .05); free iron (DC: 150.4 ± 7.07 vs. DT: 98.8 ± 7.7 µgm/gm of Hb, p < .05); TBARS (DC + H2 O2 : 24.62 ± 11.30 vs. DC + H2 O2 : 9.82 ± 2.56 mmoles/h, p < .05); carbonyl (DC: 40.40 ± 1.57 vs. DT: 25.50 ± 1.12 mmoles/g of Hb, p < .05) levels and ß-cell count/pancreatic islet (DC: 85 ± 15 vs. DT: 125 ± 20, p < .05). Thus, G. glabra extract is quite effective against hyperglycemia and the associated free iron-mediated oxidative stress. PRACTICAL APPLICATIONS: Chronic use of oral hypoglycemic synthetic drugs may produce side effects and drug resistance. Recently, various plant extracts are being researched to explore their antihyperglycemic potential. Here, the effects of this alcoholic powdered root extract on STZ-induced diabetic changes and associated oxidative stress, including hemoglobin-induced free iron-mediated oxidative reactions were examined. The STZ-induced diabetic changes and hemoglobin-glycation-induced free iron-mediated oxidative reactions were alleviated in the Wistar rats after 1-month of treatment with the extract. We have also reported previously that glycyrrhizin, a bioactive constituent of Glycyrrhiza glabra root inhibits peroxidase, esterase activities of hemoglobin and hemoglobin-mediated oxidative damage without affecting oxygen-binding capacity of the protein. This preclinical work further substantiates the potential therapeutic use of the G. glabra whole root extract in the treatment of diabetes mellitus.

Effect of ginseng therapy on diabetes and its chronic complications: lessons learned.

Ginseng played a significant role in the management of diabetes in China and in other Asian countries for a long period of time. It has a large number of pharmacological properties and is relatively free from adverse effects. As a part of Ontario Ginseng Research and Innovation Consortium, we investigated the effects of ginseng extract on diabetes and its complications. We demonstrated large number of beneficial effects of ginseng therapy and showed that these effects are possibly mediated through its antioxidant properties. Thus ginseng may lend itself as a relatively safe and inexpensive adjuvant treatment for diabetes and chronic diabetic complications.

North American Ginseng (Panax quinquefolius) prevents hyperglycemia and associated pancreatic abnormalities in diabetes.

North American ginseng (NAG) has received increasing attention as an alternative medicine for the treatment of diabetes. Extract of the NAG root has been reported to possess antidiabetic properties, but the underlying mechanisms for such effects have not been identified. Here we investigated the effects of NAG root extract on type 1 and 2 diabetes and the underlying mechanisms involved for such effects. Type 1 [C57BL/6 mice with streptozotocin (STZ)-induction] and type 2 (db/db) diabetic models were examined. Groups of diabetic mice (both type 1 and 2) were treated with alcoholic extract of the NAG root (200 mg/kg BW/day, oral gavage) for 1 or 2 months following onset of diabetes. Ginseng treatment significantly increased the body weight in type 1 diabetic animals in contrast to the type 2 model, where it caused diminution of body weight. Blood glucose and glycated hemoglobin levels diminished in the diabetic groups of both models with NAG treatment. Interestingly, plasma insulin and C-peptide levels were significantly increased in the STZ-diabetic mice, whereas they were reduced in the db/db mice following NAG treatment. Histological and morphometric analyses (islet/pancreas ratio) of the pancreas revealed an increase in the islet area following the treatment compared to both the untreated diabetic groups. These data indicate that NAG possibly causes regeneration of ß-cells resulting in enhanced insulin secretion. On the other hand, in type 2 diabetes, the additional effects of NAG on body weight might have also resulted in improved glucose control.

High glucose induced alteration of SIRTs in endothelial cells causes rapid aging in a p300 and FOXO regulated pathway.

In diabetes, some of the cellular changes are similar to aging. We hypothesized that hyperglycemia accelerates aging-like changes in the endothelial cells (ECs) and tissues leading to structural and functional damage. We investigated glucose-induced aging in 3 types of ECs using senescence associated ß-gal (SA ß-gal) staining and cell morphology. Alterations of sirtuins (SIRTs) and their downstream mediator FOXO and oxidative stress were investigated. Relationship of such alteration with histone acetylase (HAT) p300 was examined. Similar examinations were performed in tissues of diabetic animals. ECs in high glucose (HG) showed evidence of early senescence as demonstrated by increased SA ß-gal positivity and reduced replicative capacities. These alterations were pronounced in microvascular ECs. They developed an irregular and hypertrophic phenotype. Such changes were associated with decreased SIRT (1-7) mRNA expressions. We also found that p300 and SIRT1 regulate each other in such process, as silencing one led to increase of the others' expression. Furthermore, HG caused reduction in FOXO1's DNA binding ability and antioxidant target gene expressions. Chemically induced increased SIRT1 activity and p300 knockdown corrected these abnormalities slowing aging-like changes. Diabetic animals showed increased cellular senescence in renal glomerulus and retinal blood vessels along with reduced SIRT1 mRNA expressions in these tissues. Data from this study demonstrated that hyperglycemia accelerates aging-like process in the vascular ECs and such process is mediated via downregulation of SIRT1, causing reduction of mitochondrial antioxidant enzyme in a p300 and FOXO1 mediated pathway.

Preventive effects of North American ginseng (Panax quinquefolius) on diabetic retinopathy and cardiomyopathy.

Ginseng (Araliaceae) has multiple pharmacological actions because of its diverse phytochemical constituents. The aims of the present study are to evaluate the preventive effects of North American ginseng on diabetic retinopathy and cardiomyopathy and to delineate the underlying mechanisms of such effects. Models of both type 1 (C57BL/6 mice with streptozotocin-induced diabetes) and type 2 diabetes (db/db mice) and age-matched and sex-matched controls were examined. Alcoholic ginseng root (200 mg/kg body weight, daily oral gavage) extract was administered to groups of both type 1 and type 2 diabetic mice for 2 or 4 months. Dysmetabolic state in the diabetic mice was significantly improved by ginseng treatment. In both the heart and retina of diabetic animals, ginseng treatment significantly prevented oxidative stress and diabetes-induced upregulations of extracellular matrix proteins and vasoactive factors. Ginseng treatment in the diabetic animals resulted in enhancement of stroke volume, ejection fraction, cardiac output, and left ventricle pressure during systole and diastole and diminution of stroke work. In addition, mRNA expressions of atrial natriuretic factor and brain natriuretic factor (molecular markers for cardiac hypertrophy) were significantly diminished in ginseng-treated diabetic mice. These data indicate that North American ginseng prevents the diabetes-induced retinal and cardiac biochemical and functional changes probably through inhibition of oxidative stress.

Preventive effects of North American ginseng (Panax quinquefolium) on diabetic nephropathy.

PURPOSE: Ginseng has been used as an herbal medicine and nutritional supplement in East Asia for thousands of years and gained popularity in the west because of its various pharmacological properties. Panax ginseng (Asian ginseng) and Panax quinquefolium (North American ginseng) both are reported to possess antihyperglycemic properties. The aim of the present study is to evaluate the preventive effects of North American ginseng on diabetic nephropathy (DN) and the underlying mechanisms of such effects. METHODS: Models of both type 1 (C57BL/6 mice with STZ-induced diabetes) and type 2 diabetes (db/db mice) and age- and sex-matched controls were examined. Alcoholic ginseng root (200mg/kgbodywt, daily oral gavage) extract was administered to the diabetic mice (type 1 and type 2) for two or four months in order to evaluate its effects on DN. RESULTS: Dysmetabolic state in the diabetic mice was significantly improved by ginseng treatment. In the kidneys of diabetic animals, ginseng significantly prevented oxidative stress and reduced the NF-κB (p65) levels. Diabetes-induced up-regulations of ECM proteins and vasoactive factors in the kidneys were significantly diminished by ginseng administration. Furthermore, albuminuria and mesangial expansion in the diabetic mice were prevented by ginseng therapy. CONCLUSION: North American ginseng has preventive effects on DN and it works through a combination of mechanisms such as antihyperglycemic and antioxidant activities.

miR-146a-Mediated extracellular matrix protein production in chronic diabetes complications.

OBJECTIVE: MicroRNAs (miRNAs), through transcriptional regulation, modulate several cellular processes. In diabetes, increased extracellular matrix protein fibronectin (FN) production is known to occur through histone acetylator p300. Here, we investigated the role of miR-146a, an FN-targeting miRNA, on FN production in diabetes and its relationship with p300. RESEARCH DESIGN AND METHODS: miR-146a expressions were measured in endothelial cells from large vessels and retinal microvessels in various glucose levels. FN messenger RNA expression and protein levels with or without miR-146a mimic or antagomir transfection were examined. A luciferase assay was performed to detect miR-146a's binding to FN 3'-untranslated region (UTR). Likewise, retinas from type 1 diabetic rats were studied with or without an intravitreal injection of miR-146a mimic. In situ hybridization was used to localize retinal miR-146a. Cardiac and renal tissues were analyzed from type 1 and type 2 diabetic animals. RESULTS: A total of 25 mmol/L glucose decreased miR-146a expression and increased FN expression compared with 5 mmol/L glucose in both cell types. miR-146a mimic transfection prevented such change, whereas miR-146a antagomir transfection in the cells in 5 mmol/L glucose caused FN upregulation. A luciferase assay confirmed miR-146a's binding to FN 3'-UTR. miR-146a was localized in the retinal endothelial cells and was decreased in diabetes. Intravitreal miR-146a mimic injection restored retinal miR-146a and decreased FN in diabetes. Additional experiments showed that p300 regulates miR-146a. Similar changes were seen in the retinas, kidneys, and hearts in type 1 and type 2 diabetic animals. CONCLUSIONS: These studies showed a novel, glucose-induced molecular mechanism in which miR-146a participates in the transcriptional circuitry regulating extracellular matrix protein production in diabetes.

American ginseng (Panax quinquefolius) prevents glucose-induced oxidative stress and associated endothelial abnormalities.

PURPOSE: Ginseng (Araliaceae), demonstrates widespread biological effects because of its purported antioxidant and other properties. The present study was undertaken to investigate the effects of American ginseng root extract on glucose-induced oxidative stress and associated oxidative damage to human umbilical vein endothelial cells (HUVECs). METHODS: Following pretreatment with various concentrations of ginseng (alcoholic extract), HUVECs were incubated with various concentrations of d-glucose ranging from 5 to 25mmol/l for 24h. l-Glucose was used at a concentration of 25mmol/l as a control. RESULTS: Glucose-induced oxidative stress detected by intracellular reactive oxygen species accumulation, superoxide anion generation and DNA damage in HUVECs were significantly prevented by ginseng. Treatment of HUVECs with ginseng further led to significant prevention of glucose-induced NF-κB activation. Glucose-induced increase in fibronectin (FN), EDB(+)FN (a splice variant of FN), endothelin-1 (ET-1) and vascular endothelial growth factor (VEGF) mRNAs and protein levels were also prevented by ginseng treatment. CONCLUSION: These data indicate that American ginseng prevented glucose-induced damage in the HUVECs through its antioxidant properties.

Ameliorative effects of glycyrrhizin on streptozotocin-induced diabetes in rats.

OBJECTIVES: Glycyrrhizin is the main water-soluble constituent of the root of liquorice (Glycyrrhiza glabra). The study investigates the effect of glycyrrhizin on streptozotocin (STZ)-induced diabetic changes and associated oxidative stress, including haemoglobin-induced free iron-mediated oxidative reactions. METHODS: Male Wistar rats were grouped as normal control, STZ-induced diabetic control, normal treated with glycyrrhizin, diabetic treated with glycyrrhizin and diabetic treated with a standard anti-hyperglycaemic drug, glibenclamide. Different parameters were studied in blood and tissue samples of the rats. KEY FINDINGS: Glycyrrhizin treatment improved significantly the diabetogenic effects of STZ, namely enhanced blood glucose level, glucose intolerant behaviour, decreased serum insulin level including pancreatic islet cell numbers, increased glycohaemoglobin level and enhanced levels of cholesterol and triglyceride. The treatment significantly reduced diabetes-induced abnormalities of pancreas and kidney tissues. Oxidative stress parameters, namely, serum superoxide dismutase, catalase, malondialdehyde and fructosamine in diabetic rats were reverted to respective normal values after glycyrrhizin administration. Free iron in haemoglobin, iron-mediated free radical reactions and carbonyl formation in haemoglobin were pronounced in diabetes, and were counteracted by glycyrrhizin. Effects of glycyrrhizin and glibenclamide treatments appeared comparable. CONCLUSION: Glycyrrhizin is quite effective against hyperglycaemia, hyperlipidaemia and associated oxidative stress, and may be a potential therapeutic agent for diabetes treatment.

Leptin and endothelin-1 mediated increased extracellular matrix protein production and cardiomyocyte hypertrophy in diabetic heart disease.

BACKGROUND: We investigated the role of leptin and its interaction with endothelin 1 (ET-1) in fibronectin (FN) synthesis and cardiomyocyte hypertrophy, two characteristic features of diabetic cardiomyopathy. METHODS: Endothelial cells [human umbilical vein endothelial cells (HUVECs)] were examined for FN production and neonatal rat cardiomyocytes for hypertrophy, following incubation with glucose, ET-1, leptin and specific blockers. FN, ET-1, leptin and leptin receptors mRNA expression and FN protein were measured. Myocytes were also morphometrically examined. Furthermore, hearts from streptozotocin-diabetic rats were analysed. RESULTS: Glucose caused increased FN mRNA and protein expression in HUVECs and cardiomyocytes hypertrophy along with upregulation of ET-1 mRNA, leptin mRNA and protein. Glucosemimetic effects were seen with leptin and ET-1. Leptin receptor antagonist (leptin quadruple mutant) and dual endothelin A endothelin B (ETA/ETB) receptor blocker bosentan normalized such abnormalities. Hearts from the diabetic animals showed hypertrophy and similar mRNA changes. CONCLUSION: These data indicate that in diabetes increased FN production and cardiomyocyte hypertrophy may be mediated through leptin with its interaction with ET-1.

Action of pelargonidin on hyperglycemia and oxidative damage in diabetic rats: implication for glycation-induced hemoglobin modification.

Glycation-modified hemoglobin in diabetes mellitus has been suggested to be a source of enhanced catalytic iron and free radicals causing pathological complications. The present study aims to verify this idea in experimental diabetes. Pelargonidin, an anthocyanidin, has been tested for its antidiabetic potential with emphasis on its role against pathological oxidative stress including hemoglobin-mediated free radical reactions. Male wistar rats were grouped as normal control, streptozotocin-induced diabetic control, normal treated with pelargonidin and diabetic treated with pelargonidin. Pelargonidin-treated rats received one time i.p injection of the flavonoid (3 mg/kg bodyweight). Biochemical parameters were assayed in blood samples of different groups of rats. Liver was used for histological examinations. Pelargonidin treatment normalized elevated blood glucose levels and improved serum insulin levels in diabetic rats. Glucose tolerance test appeared normal after treatment. Decreased serum levels of SOD and catalase, and increased levels of malondialdehyde and fructosamine in diabetic rats were reverted to their respective normal values after pelargonidin administration. Extents of hemoglobin glycation, hemoglobin-mediated iron release, iron-mediated free radical reactions and carbonyl formation in hemoglobin were pronounced in diabetic rats, indicating association between hemoglobin glycation and oxidative stress in diabetes. Pelargonidin counteracts hemoglobin glycation, iron release from the heme protein and iron-mediated oxidative damages, confirming glycated hemoglobin-associated oxidative stress in diabetes.

Effect of non-enzymatic glycation on esterase activities of hemoglobin and myoglobin.

Heme proteins--hemoglobin and myoglobin possess esterase activities. Studies with purified hemoglobin from normal individuals and diabetic patients revealed that the esterase activity as measured from hydrolysis of p-nitrophenyl acetate (p-NPA) was higher in diabetic condition and increased progressively with extent of the disease. HbA(1c), the major glycated hemoglobin, which increases proportionately with blood glucose level in diabetes mellitus, exhibited more esterase activity than the non-glycated hemoglobin fraction, HbA(0), as demonstrated spectrophotometrically as well as by activity staining. Glycation influenced esterase activity of hemoglobin by increasing the affinity for the substrate and the rate of the reaction. Both HbA(0) and HbA(1c)-mediated catalysis of p-NPA hydrolysis was pH-dependent. Esterase activity of in vitro-glycated myoglobin (GMb) was also higher than that of its non-glycated analog (Mb). The amplified esterase activities of hemoglobin and myoglobin might be associated with glycation-induced structural modifications of the proteins.

Effect of nonenzymatic glycation on functional and structural properties of hemoglobin.

HbA(1c), the major glycated hemoglobin increases proportionately with blood glucose concentration in diabetes mellitus. H(2)O(2) promotes more iron release from HbA(1c) than that from nonglycated hemoglobin, HbA(0). This free iron, acting as a Fenton reagent, might produce free radicals and degrade cell constituents. Here we demonstrate that in the presence of H(2)O(2), HbA(1c) degrades DNA and protein more efficiently than HbA(0). Formation of carbonyl content, an index of oxidative stress, is higher by HbA(1c). Compared to HbA(0), HbA(1c) is more rapidly autooxidized. Besides these functional changes, glycation also causes structural modifications of hemoglobin. This is demonstrated by reduced alpha-helix content, more surface accessible hydrophobic tryptophan residues, increased thermolability and weaker heme-globin linkage in HbA(1c) than in its nonglycated analog. The glycation-induced structural modification of hemoglobin may be associated with its functional modification leading to oxidative stress in diabetic patients.

In vitro nonenzymatic glycation enhances the role of myoglobin as a source of oxidative stress.

Metmyoglobin (Mb) was glycated by glucose in a non-enzymatic in vitro reaction. Amount of iron release from the heme pocket of myoglobin was found to be directly related with the extent of glycation. After in vitro glycation, the unchanged Mb and glycated myoglobin (GMb) were separated by ion exchange (BioRex 70) chromatography, which eliminated free iron from the protein fractions. Separated fractions of Mb and GMb were converted to their oxy forms -MbO2 and GMbO2, respectively. H2O2-induced iron release was significantly higher from GMbO2 than that from MbO2. This free iron, acting as a Fenton reagent, might produce free radicals and degrade different cell constituents. To verify this possibility, degradation of different cell constituents catalyzed by these fractions in the presence of H2O2 was studied. GMbO2 degraded arachidonic acid, deoxyribose and plasmid DNA more efficiently than MbO2. Arachidonic acid peroxidation and deoxyribose degradation were significantly inhibited by desferrioxamine (DFO), mannitol and catalase. However, besides free iron-mediated free radical reactions, role of iron of higher oxidation states, formed during interaction of H2O2 with myoglobin might also be involved in oxidative degradation processes. Formation of carbonyl content, an index of oxidative stress, was higher by GMbO2. Compared to MbO2, GMbO2 was rapidly autooxidized and co-oxidized with nitroblue tetrazolium, indicating increased rate of Mb and superoxide radical formation in GMbO2. GMb exhibited more peroxidase activity than Mb, which was positively correlated with ferrylmyoglobin formation in the presence of H2O2. These findings correlate glycation-induced modification of myoglobin and a mechanism of increased formation of free radicals. Although myoglobin glycation is not significant within muscle cells, free myoglobin in circulation, if becomes glycated, may pose a serious threat by eliciting oxidative stress, particularly in diabetic patients.

Human papillomavirus infection among Indian mothers and their infants.

OBJECTIVE: Several studies have demonstrated that infants can acquire human papillomavirus (HPV) infection at birth from their mothers. The aim of the present investigation was to determine prevalence of HPV infection among pregnant women and evaluate the extent of perinatal transmission of HPVs to infants. METHODS: The study included 135 pregnant women and their infants. The polymerase chain reaction (PCR) was performed to detect HPV DNA in cervical cells of the women and buccal cells of the infants. RESULTS: HPVs detected were genotyped by PCR using type specific primers. HPV DNA was identified in 38 mothers (28.14%, 38/135) and 14 babies (10.37%, 14/135). The prevalence rate of HPV type 16 was highest both in HPV positive maternal (63.15%, 24/38) and baby samples (85.71%, 12/14). At birth, the frequency of HPV transmission from infected mothers to their infants was 18.42% (7/38). The proportion of infants with HPV infection delivered by cesarean section was 78.57% (11/14). CONCLUSION: Cesarean section was not found protective for infants against perinatal HPV transmission. Infection in the infants was cleared within one year. This is the first report of its kind from India.