Human Herpes Virus 6 & 7 in Pityriasis Rosea

Background: Pityriasis rosea (PR) is a common papulosquamous skin disease in which infective agent may be implicated. Reactivation of human herpes virus 7 (HHV-7) and, in some cases human herpes virus 6 (HHV-6) was suggested to occur in PR. Objective: The objective of this case control study was to detect a possible role of both HHV-7 and HHV-6 in the aetiology of PR by polymerase chain reaction (PCR) of both serum and skin lesions. Subjects and methods: This work was achieved through the study of 22 patients (9 males, 13 females, age ranged from 14 to 42 years), 13 age and sex matched patients with other dermatological diseases (4 psoriasis vulgaris, 3 lichen planus, 3 alopecia areata and 3 acne vulgaris) and 8 age and sex matched healthy control. Serum samples were taken from all patients and control. Punch biopsies were taken from lesional skin of both patient groups and from non lesional skin of PR patients, put in saline. Serum and skin biopsies were stored at -70°c until the time of nested PCR for both HHV-6 and HHV-7. Results: HHV-6 was detected by PCR in 7/22 (31.82%) lesional skin, in 5/22 (22.73%) of non lesional skin and in 5/22 (22.73%) of serum samples in PR patients. In the group of other dermatologic diseases HHV-6 was detected in 1/13 (7.69%) of lesional skin and 1/13 (7.69%) of serum samples of one case of psoriasis vulgaris. HHV-7 was detected by PCR in 10/22 (45.45%) of lesional skin, 6/22 (27.27%) of non-lesional skin and 7/22 (31.81%) of serum samples in PR patients. HHV-7 was detected in only one 1/8 (12.5%) serum sample of the healthy control. Conclusion: HHV-6 and HHV-7 may play a part in the pathogenesis of PR in some patients.

Human Herpes Virus 6 & 7 in Pityriasis Rosea

Yousry M Moustafa and Sahar Taher*

Departments of Dermatology & Andrology and Medical Microbiology & Immunology*, Mansoura Faculty of Medicine, Mansoura

Abstract

Background: Pityriasis rosea (PR) is a common papulosquamous skin disease in which infective agent may be implicated. Reactivation of human herpes virus 7 (HHV-7) and, in some cases human herpes virus 6 (HHV-6) was suggested to occur in PR. Objective: The objective of this case control study was to detect a possible role of both HHV-7 and HHV-6 in the aetiology of PR by polymerase chain reaction (PCR) of both serum and skin lesions. Subjects and methods: This work was achieved through the study of 22 patients (9 males, 13 females, age ranged from 14 to 42 years), 13 age and sex matched patients with other dermatological diseases (4 psoriasis vulgaris, 3 lichen planus, 3 alopecia areata and 3 acne vulgaris) and 8 age and sex matched healthy control. Serum samples were taken from all patients and control. Punch biopsies were taken from lesional skin of both patient groups and from non lesional skin of PR patients, put in saline. Serum and skin biopsies were stored at -70°c until the time of nested PCR for both HHV-6 and HHV-7. Results: HHV-6 was detected by PCR in 7/22 (31.82%) lesional skin, in 5/22 (22.73%) of non lesional skin and in 5/22 (22.73%) of serum samples in PR patients. In the group of other dermatologic diseases HHV-6 was detected in 1/13 (7.69%) of lesional skin and 1/13 (7.69%) of serum samples of one case of psoriasis vulgaris. HHV-7 was detected by PCR in 10/22 (45.45%) of lesional skin, 6/22 (27.27%) of non-lesional skin and 7/22 (31.81%) of serum samples in PR patients. HHV-7 was detected in only one 1/8 (12.5%) serum sample of the healthy control. Conclusion: HHV-6 and HHV-7 may play a part in the pathogenesis of PR in some patients.

Introduction

Pityriasis rosea (PR) is a common papulosquamous skin disease with unknown aetiology⁽¹⁾. Many epidemiological and clinical features suggest that an infective agent may be implicated. Epidemiological evidence for infectivity includes occasional family or household outbreaks, seasonal and year-to-year fluctuations⁽²⁾, statistical evidence for clustering in space and time⁽³⁾, and significantly commoner respiratory infection in PR patients than control⁽⁴⁾. Earlier suspicions about fungi, streptococci and spirochaetes have not been confirmed⁽³⁾. A possible picorna virus was detected on culture of scale or of skin biopsy from a minority of patients⁽⁵⁾.

Human herpsviruses 6 and 7 belong to the genus Roseolavirus within the subfamily Betaherpesvirinae. These ubiquitous viruses may cause primary or chronic persistent infection or remain in a state of latency for many years, until a decrease in the immunologic state of the host leads to reactivation of infection. Several diseases have been linked with HHV-6 and HHV-7⁽⁶⁾. In 1997, a link between PR and the reactivation of human herpes virus (HHV)-7 infection, an ubiquitous β-herpes virus, was first described^(7,8). Contrasting results were, however, obtained in subsequent studies. Several authors were unable to confirm the orginal finding of HHV-7 both in adult and children with PR^(9,10,11,12), whereas others suggested that reactivation of HHV-7 and, in some cases HHV-6, may occur in PR^(13,14).

Additional evidence in support of the involvement of HHV-7 and/or HHV-6 in PR came from the detection of herpes virus-like particles in PR lesional skin⁽¹⁵⁾. PR was reported to be associated with active systemic co-infection with both HHV-6 and HHV-7⁽¹⁶⁾.

Therefore, this study was aimed to detect a possible role of both HHV-7 and HHV-6 in the aetiology of PR by PCR of both serum and skin lesions.

Subjects and Methods

This study included 22 selected pityriasis rosea patients (9 males and 13 females) attending the Outpatient Clinic of Dermatology Andrology Mansoura University Hospitals from July 2008 to November 2008. Their ages ranged from 14 to 42 years (mean 27.9 ± 8.1). We selected patients with history of eruption dating one or two weeks. Thirteen age (13-46 years mean 29.9 ± 11.2 years) and sex matched patients with different skin disease (4 psoriasis vulgaris, 3 lichen planus, 3 Alopecia areata, and 3 acne vulgaris) served as dermatologic control.

Also eight age (15-40 years, mean 31.0 ± 9.4) and sex matched healthy individuals (3 males & 5 females) served as healthy control.

All patients and the two control groups were subjected to thorough history taking about duration of pityriasis rosea history of consititutional symptoms in patients and we excluded control giving past history of eruption similar to pityriasis rosea. The patients with pityriasis rosea were examined clinically for the number and distribution of the lesions and the type of pityriasis rosea.

Five ml of venous blood were taken from every one of patients and control put on plain tube and centrifuged for 30 minutes at 1000 RPM and serum was stored at -70°C until the time of PCR.

From every patient with pityriasis rosea two punch biopsies were taken, one from the lesion and the other one from non lesional skin, punch biopsy was taken from lesional skin of each one of dermatologic control. Each of lesional biopsies of patients with PR were divided into two equal halves, one half put in formalin and embedded in paraffin for histopathological examination to confirm the clinical diagnosis. The other half, as well as, the non lesional biopsies of PR patients and lesional biopsies of dermatologic control were put in saline and stored at -70°C until the time of PCR.

DNA preparation and detection of HHV-6 and HHV-7 DNA by nested PCR

The primers sets used for nested PCR to amplify human herpes virus 6 and 7 DNA sequences (5¢-3¢) are shown in Table (1) as described by Watanabe et al.⁽¹⁶⁾. DNA extraction from skin biopsy was done by the use of QIA Amp Kit (Qiagen Hilden, Germany). Twenty µL Qiagen protease were pipetted into the bottom of a microcentrifuge tube. Two hundred µL of samples after grinding with tissue grinder in phosphate buffer saline (PBS) and buffer AL (200 µL), were added and mixed by pulse vortexing for 15 seconds. The mixture was incubated at 56°c for 10 minutes, then 200 µL ethanol were added and mixed. The mixture was applied to the spin column and centrifuged at 8000 rpm for 1 minute. Five hundred µL of AW2 were applied and centrifuged at 14000 rpm for 3 minutes was done. Spin column was placed in microcentrifuge tube and collection tube containing the filtrate was discarded. Two hundred buffer AE was added, incubation at room temperature and centrifugation were done. A second step with 200 µL AE buffer will increase yields by up to 15% (Watanabe et al.⁽¹⁶⁾).

DNA amplification by nested PCR, 2 rounds of amplification were done. In the first round of amplification, 1 µL of each nucleotide primers. Two µL of each DNA preparation, I µL of sense primer, 1 µL of antisense primer were added to 46 µL of master mix containing 3 µL MgCI₂ solution, 5 µL X PCR buffer (100mM Tris HCI (pH 8.3), 500 mM KCI/ µL), 1 µL NTPs mixture (10mM/ µL), 0.4 µL Ampli Taq DNA Polymerase (5 units/ml) all in 36.6 µL distilled water. The reaction was overlaid with mineral oil. After an initial denaturation step of 5 mintutes at 94°C, 38 cycles were performed at 94°C for 45 seconds, 54°C for 45 seconds and 72°C for 1 minute.

After the first round of amplification, 2 µL of the first PCR product was added to the second round PCR mixture with 1 µL of each internal primers 5.

Thirty five cycles of amplification using the cycling parameters were performed. Subsequently, the nested PCR products of size 264-bp for HHV-6 and 186-bp for HHV-7 were confirmed on 2% agarose gel and stained with ethidium bromide in comparison to molecular size marker (f X 174 DNA/ Hae III).

Nested PCR for serum samples was done as described by the manufacturer. 

Statistical analysis

Data were analyzed using SPSS (statistical package for social science) version 11. Qualitative variables were presented as number and percentage %). Kolomogrov-Smirov test was used to test for normaly distribution of these variables. Normally distributed variables were presented as mean ± standard deviation (SD) and student (t) test and one way ANOVA (F) tests were used for two groups and more than two groups comparison, respectively. Non parametric variables were presented as median and range and Mann-Whitney (z) and Kruskal-Wallis (KWX₂) tests were used for two groups and more than two groups comparison, respectively. Fisher exact test was used for comparing the results of nested PCR between the studied groups. P≤ 0.05 was considered to be statistically significant.

Results

The duration of PR was one week in 8 patients and 2 weeks in 14 patients, constitutional symptom were present in 9 patients 4 of them was positive for both HHV-6 & HHV-7. Classic type was found in 15 patients and inverted type was found in 7 patients.

In this study HHV-6 was detected by PCR in 7 out of 22 lesional biopsies of PR patients (31.82%), in 5 (21.73%) of the non-lesional 22 punch biopsies and in 5 (22.73%) serum samples of the same PR patient group. In the group 2 of other dermatologic diseases, only one punch biopsy of lesional skin in case of psoriasis vulgaris and serum of the same patient was positive for HHV-6 1/13 (7.69%). All skin and serum samples of the control group were negative for HHV-6 (Table 2 & Fig. 1).

HHV-7 was detected by PCR in 10 lesional skin biopsies (45.45%), 6 non-lesional skin biopsies (27.27%) and 7 (31.81%) serum samples in the 22 PR patients group. All lesional, biopsies and serum samples of group 2 of other dermatologic diseases were negative for HHV-7. In the control group only one serum sample 1/8 (12.5%) was positive for HHV-7 by PCR (Table 2 & Fig. 2).

Table 1.    Primer sequences used for nested PCR detection for HHV-6 and HHV-7.

Table 2.    Nested PCR detection of HHV-6 and HHV-7 in studied subjects.

Fet= Fisher exact test, * Significant P value

Table 3.    Clinical manifestation of PR patients with positive nested PCR results.

All samples= lesional, non-lesional skin and serum.

Fig. 1.            Showing (M) marker in lane 1 and positive nested PCR samples for HHV-6 in lanes 5, 6, 8 and 10.

Fig. 2.            Showing (M) marker in lane 1 and positive nested PCR samples for HHV-7 in lanes 2, 3, 6, 8, 9 and 10.

Discussion

Pityriasis rosea is a papulosquamous disease in which many epidemiological and clinical features suggest a viral pathogenesis. They include preferential occurrence of PR in spring, fever as prodromal symptom, herald patch followed by secondary eruption, characteristic distribution, spontaneous regression of skin lesions and recurrences during immunosuppression, as is often observed in patients with viral diseases^(1,18,19). In our study HHV-6 was detected by nested PCR in 7/22 (31.82%) of lesional skin, 5/22 (22.72%) of non-lesional skin and 5/22 (22.73%) serum samples of PR patients. HHV-6 was detected in only 1/13 (7.69%) lesional skin and 1/13 (7.69%) serum samples of dermatologic controls. No HHV-6 sequences were detected in healthy control. HHV-7 was detected in 10/22 (45.45%), of lesional skin, 6/22 (27.27%) of non lesional skin and 7/22 (31.81%) of serum samples of PR patients. No HHV-7 sequences were detected in dermatologic control while only one serum samples 1/8 (12.5%) of healthy control was positive. These results were against those of Drago et al^(7,8), who have found HHV-6 in 6/12 (50%) in peripherial blood mononuclear cells (PBMC) in PR patients and   6/25 (24%) of control. They detected HHV-7 in 12/12 (100%) in skin, plasma and PBMC in PR versus 0% in skin and plasma of control but they found HHV-7 in 11/25 (44%) of controls. The difference between our results and that of Drago et al^(7,8), may be explained by the differences in patients populations, number of patients and the fact that both HHV-7 and HHV-6 are known to infect and reside in circulating CD4+ lymphocytes. These cells are the likely source of cell free viral DNA found in sera of PR patients. CD4+ lymphocytes, after migrating to the skin, are the likely source of both HHV-6 and HHV-7 in the skin lesions^(20,21,22).

Watanabe et al,⁽²³⁾ detected HHV-7 sequences in only about 17/36 (50%) of plasma samples of PR patients and did not detect HHV-7 sequences in the 31 plasma samples of control. These results were near to our results as regard HHV-7 in serum and against that of Drago et al^(7,8). In another study done Watanabe et al⁽¹⁶⁾, they had detected HHV-7 DNA sequences in 13/14 (93%) of lesional skin, 12/14 (86%) of non lesional skin, 10/10 (100%) of saliva, 10/12 (83%) of PBMC and 8/8 (100%) serum samples. The percentage for detecting HHV-6 DNA in these samples were, 86% (12/14) of lesional skin, 79% (11/14) of non lesional skin, 80% (8/10) of saliva, 83% (10/12) of PBMC and 88% (7/8) of serum samples. They concluded on the base of these high percentage of positive cases by nested PCR for both HHV-7 and HHV-6 that PR is associated with systemic active infection with both HHV-7 and HHV-6. Yoshida⁽²⁴⁾, have found HHV-7 in 100% (4/4) in PR and 100% (3/3) of healthy control by applying nested PCR protocol to peripheral blood DNA. This finding argues against an increase in viral DNA load in the PBMC of patients with PR and against the specific occurrence of the viral sequences in the PR samples. But, Drago et al⁽²⁵⁾, reported that the whole blood is not the same substrate as PBMC or plasma, and using it may lead to incorrect conclusions. Yasukawa et al⁽¹³⁾. Detected HHV-6 genomes in 43% (6/14) in PBMC, a percentage near to our study in skin lesion (31.82%). They detected HHV-7 genomes in only 7% (1/14) in PBMC, This is far lower than our positive cases in lesional, non-lesional skin and serum samples as regard HHV-7. They suggested that marked viral replication did not occur in PR, and a lack of association between PR and HHV-7 infection. However they suggest that HHV-6 is reactivated in some patients with PR.

Another study against our results was done by Kempf et al⁽⁹⁾ who had detected HHV-7 in only 1 of 13 (8%) skin biopsies of PR lesions versus 2 of 14 (14%) of normal skin of control. They concluded that low detection rate of HHV-7 argues strongly against a causative role of HHV-7 in the pathogenesis of PR. In a study conducted by Kosuge et al⁽¹⁰⁾ a percentage of positive cases for HHV-6 of 29 (21%) and HHV-7 13 of 30 (43%) of PBMC samples was detected. These results were near to our positive cases in lesional, non lesional skin and serum of PR patients. They reported higher positive cases in control than our study 14 of 25 (56%) in HHV-7 and 9 of 23 (39%) in HHV-6. They concluded that HHV-7 and HHV-6 may play a part in some patients with PR, but other causative agents may exist. Offidani et al⁽²⁶⁾ investigated the presence of HHV-7 in several body samples such as urine, saliva, PBMC and scales from 12 patients with active PR in parallel with 20 healthy controls. They detected HHV-7 DNA sequences only in saliva samples of five patients and 14 controls. While PBMC, urine and scales of lesional skin of PR and scrapping from skin of control were all negative for HHV-7. These findings could not support the idea of a correlation between HHV-7 and PR. In a study done by Akar et al.⁽²⁷⁾ HHV-6 DNA sequences were detected in 8 of 32 (25%) skin samples of patients with PR, while plasma and PBMC samples were negative. HHV 6 DNA was found in 1 of 15 skin samples of patients with other dermatoses. These results agree with our results of lesional skin of PR patients 7/22 (31.82%) and other dermatosis 1/13 (7.69%) but disagree with our one as regard serum samples. Also our results of HHV-7 disagree with that of Akar et al⁽²⁷⁾ who did not detect HHV-7 DNA in skin lesions, plasma or PBMC of any patient with PR. They concluded that HHV-6 DNA positivity in primary and secondary lesions may suggest that the HHV-6 may play a part in pathogenesis of some patients with PR. Broccolo et al⁽²⁸⁾ have reported that HHV-7 and less frequently, HHV-6 are active during the early stage of PR, suggesting that they might play, both in adults and children, an etiological role in this disease. They have shown that HHV-6 and HHV-7 plasma load, a direct marker of viral replication, is associated with the development of systemic symptoms as well as with a significant reduction of the humoral neutralizing response against HHV-7, further suggesting that PR may be because of the endogenous reactivation of HHV-7 and or HHV-6 infection. Although Drago et al reported an association between HHV-7 and PR^(7,8), these investigators did not document an additional role for HHV-6 in this disease, nor did they localize virus within PR skin lesions^(7,8).

Furthermore, reported studies on PR and HHV-7 following the initial report by Drago et al^(7,8) did not find evidence for association between PR and HHV-7^{(9,10,12,13,23,27,29)}. Most of these negative studies that failed to find HHV-7 DNA in lesional PR tissue, plasma or serum did not use nested PCR and /or extracted DNA from formalin-fixed paraffin-embedded tissue, methods that may have led to the negative results^{(9,10,12,13,29)}. Regarding HHV-6 many studies suggested a causal link to PR^{(13,14,15,16)}.

Because of the disparate findings in the literature and the high degree of genetic similarity between HHV-7 and HHV-6, we were extremely cautious in our selection of virus specific primer sets. Our results provide firm evidence that both HHV-7 and HHV-6 were reactivated in patients with PR. This evidence was supported by recent study done by Canoplat et al⁽³²⁾ who have found HHV-6 and HVV-7 DNA sequences in blood and skin samples of PR patients. The number and percentage of positive cases in that study were near to our one and they concluded a possible role for HHV-6 and especially HHV-7 in a group of turkish patients but other aetiological factors may exist. Interestingly HHV-7 reactivation has been reported to trigger reactivation of HHV-6^(14,30,31), although the reverse has not been described. Because of this, we hypothesize that HHV-7 reactivation is able to subsequently reactivate HHV-6 in patients with PR. Our results of lower frequency of detection of HHV-6 (31.82%) in PR tissue compared to HHV-7 (45.45%), supports this hypothesis. Until now, it remain unclear what triggers active HHV-7 infection. This question will be a focus of further studies on PR⁽¹⁶⁾. Our findings suggest an association between PR and both HHV-7 and HHV-6 infections. In our results the seven positive cases for HHV-6 in lesional skin were also positive for HHV-7. Based on the number of positive cases for HHV-6 and HHV-7 in our results and from the previous discussion we can conclude that HHV-6 and HHV-7 may play a part in the pathogenesis of PR in some patient. Future studies on possible trigger (s) for HHV-6 and HHV-7 reaction in PR patients and antiherpesviral therapeutic studies should be designed to hasten recovery from PR.

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فيروس الهربس البشري السادس والسابع في النخاله الورديه

يسري محمد مصطفي - سحر طاهر*

من قسمي الجلدية والتناسلية وطب الذكوره والميكروبيولوجيا والمناعه الطبيه*بكلية الطب- جامعة المنصورة

تعتبر النخاله الورديه مرض جلدي حبيبي متحرشف ربما يكون هناك عامل معدي مسبب له. وقد كان هناك اقتراح بأن إعادة النشاط للهربس البشري السابع وفي بعض الحالات الهربس البشري السادس يمكن ان يحدث في النخاله الورديه. وقد تم عمل هذا البحث لكشف الدور المحتمل لكل من الهربس البشري السابع والسادس كسبب للنخاله الورديه بواسطة تفاعل البلمره المتسلسل العشي لكل من المصل والجلد المصاب. وتم عمل هذا البحث علي اثنتي وعشرون مريضاً بالنخاله الورديه (9 ذكور 13 إناث تتراوح أعمارهم بين 14 و42 عاماً) وثلاث عشرة من مرضي متماثلين في العمر والجنس يعانون من أمراض جلديه أخري (4 بالصدفيه الشائعه و3 بالحزاز و 3 بالثعلبه و3 بحب الشباب) وثمانية من الأصحاء المتماثليين في العمر والجنس كمجموعه ضابطه. وتم أخذ عينات المصل من كل المرضي والمجموعه الضابطه.

وتم اخذ عينات جلديه من مكان المرض ومن المكان السليم لمجموعه المرضي بالنخاله الوردية ومن مكان المرض لمجموعة الامراض الجلدية وتم وضعها في محلول ملح. وتم تخزين عينات المصل والجلد تحت درجة حرارة -70° مئوية لحين عمل تفاعل البلمره المتسلسل العشي لكل من الهربس البشري السادس والسابع. وتم الكشف عن وجود الهربس البشري السادس في 7/22 (31,82%) من عينات الجلد المصاب وفي 5/22 (22,73%) من عينات الجلد الغير مصاب وفي 5/22 (22,73%) من عينات المصل في مرضي النخاله الورديه اما في مجموعه الامراض الجلديه الأخري فتم الكشف عن وجود الهربس البشري السادس في حاله واحده 1/13 (7,69%) من الجلد المصاب والمصل. وتم الكشف عن وجود الهربس البشري السابع في 10/22 (45,45%) من عينات الجلد المصاب و6/22 (27,27%) من عينات الجلد الغير مصاب و7/22 (31,81%) من عينات المصل في مرضي النخاله الورديه بينما تم الكشف عن وجود الهربس البشري السابع في عينه واحده من عينات المصل في المجموعه الضابطه 1/8 (12,5%). ومن هذا البحث نستنتج ان الهربس البشري السادس والهربس البشري السابع ربما يلعبان دوراً في جزء من نشوء المرض في بعض المرضي بالنخاله الورديه.