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Pityriasis Rosea and Viral Infection


Pityriasis rosea (PR) is an acute inflammatory erythema, papule, scaly skin disease. The main symptom of this disease is oval or round red or yellowish brown patches on the skin. It occurs in the trunk and the proximal end of the limbs. There are usually mother spots, and in a period of 1 to 2 weeks, there is a generalized batch of rash similar to the mother spot. The long axis of the rash is consistent with the direction of the dermatoglyph. Consciously itching. Pityriasis rosea is self-limiting. It usually resolves itself after 4 to 6 weeks of rash, leaving temporary hypopigmentation or pigmentation spots. A small number of illnesses can be extended to more than half a year to heal. Scottish dermatologist Willam first reported ring-shaped rose rash in 1798 and considered it to be an independent disease. In 1860, the French dermatologist Gilbert was named Pityriasis rosea based on the clinical features of the disease and has been used to date. The etiology and pathogenesis of pityriasis rosea have not yet been elucidated. At present, there are various theories such as viral infection, allergy, autoimmunity and hereditary allergy. Among them, the study of viral infection theory is the most extensive and the most likely. The author reviews the pathogenesis of pityriasis rosea virus infection as follows.

1. Clinical epidemiological studies show that viral infection plays an important role in the pathogenesis

Clinical epidemiology has certain characteristics. The disease is more common in clinical practice, the population incidence rate is about 0.5% to 2.0%, no obvious racial differences; the age of onset varies from 3 months to 83 years, mostly in youth and adults, but there are about 75% of pityriasis rosea At the age of 10 to 30 years of age, the average age of onset is 22.7 years, and the incidence rate is similar for men and women or slightly higher for women. The onset of the disease has a certain seasonality in the spring and autumn, which is prone to viral infection. Pityriasis rosea has a cluster disease, such as family, school, military camp or public bath, and other population-intensive people have a higher incidence; some patients have prodromal symptoms such as headache, fever, joint pain, etc., in line with the characteristics of viral infection; Spot, while the mother spot can appear in the traumatic part (such as the insect bite), followed by multiple disseminated erythema, scales; the course of disease is self-limiting, usually about 4 to 6 weeks after the rash is self-resolving, can be left temporarily Hypogonadism or pigmentation spots; less recurrence. All of the above are consistent with the manifestations of disease manifestations of infection, especially viral infection. Chuh et al. searched for nearly 60 years of relevant literature analysis and concluded that the prevalence of pityriasis rosea, the epidemiology of small pandemic and clustering, which provides strong evidence for the involvement of viral infection in pityriasis rosea, its main age For the age of 10 to 35, it is suggested that the incidence is related to the primary infection and endogenous activation of the virus. The low recurrence rate is also an epidemiological marker of viral infection. There are many studies on the infection of pityriasis rosea caused by pathogenic microorganisms, and some people suspect that it is related to factors such as bacterial, fungal or parasitic infections, but there is no clear evidence that pityriasis rosea is a disease caused by a single pathogen infection.

2. Evidence of viral infection in the investigation of pityriasis rosea

Pityriasis rosea usually has a history of upper respiratory tract infection before rash. Mubki et al reported a case of pityriasis rosea in patients with influenza A. It is speculated that the influenza A virus may be the cause of pityriasis rosea, or it may activate other viruses to cause pityriasis rosea. Chuh used PCR and serology to detect cytomegalovirus (CMV), Epstein-Barr virus, parvovirus B19 DNA and antiviral antibodies in 12 patients with pityriasis rosea and 12 healthy controls. No viral DNA was detected in the case group, and the antibody titer of the three viruses was not significantly different from the control group. Anti-cytomegalovirus and anti-EBV IgM were detected in 2 patients. According to other studies, IgM in these 2 patients was caused by cross-reaction. There was no significant correlation between the onset of pityriasis rosea and the infection of cytomegalovirus, Epstein-Barr virus, and parvovirus B19. There is evidence that picornavirus, influenza and parainfluenza viruses, Legionella, Chlamydia and Chlamydia infections are also not associated with pityriasis rosea. Drago et al. compared serum IFN-γ in patients with pityriasis rosea and healthy controls, and found that the level of IFN-γ in the serum of patients with pityriasis rosea was significantly higher than that of healthy volunteers, which provided evidence for the involvement of viral infection in pityriasis rosea. IFN-γ has a direct antiviral activity, which may be caused by the secretion of NK cells and T cells by the body after invasion by pathogens such as viruses.

Recently, more and more evidence suggests that human herpesvirus plays an important role in the pathogenesis of pityriasis rosea. The study on the viral infection theory of pityriasis rosea has focused on human herpesvirus (HHV)-6 and HHV-7. In 1997, Drago et al. used electron microscopy and PCR to detect HHV-7 in monocytes, plasma and skin of patients with pityriasis rosea. The levels of interferon-α and interferon-γ in serum were detected by ELISA. The cultured peripheral blood mononuclear cells were observed for morphological changes, and the virus particles were identified under electron microscope. PCR samples were used to analyze whether all samples contained HHV-6 and HHV-7 DNA sequences. The results showed that interferon-α and interferon-γ were detected in the plasma of patients with pityriasis rosea, but not in the plasma of the control group. Peripheral monocytes isolated from patients with pityriasis rosea were cultured in vitro. After 7 days, balloon-like cells and inclusion bodies were observed under light microscope, and no such findings were found in the control group and the convalescent patients with pityriasis rosea. The supernatant obtained by centrifugation of the medium enabled the reproduction of HHV-7-replicating Sup-T1 cells; Observed, the supernatant found particles with herpes virus characteristics. The DNA sequence of HHV-7 can be detected in peripheral blood mononuclear cells, plasma and skin of patients with acute pityriasis rosea. The above findings are highly suggestive of viral activity. Although the virus has not been isolated from patients with pityriasis rosea, studies have shown that the virus plays an important role in its pathogenesis. Therefore, it is suggested that pityriasis rosea may be a clinical manifestation of HHV-7 reactivation. Chuh et al. detected the peripheral blood mononuclear cells, serum and maternal plaque DNA of 8 patients with pityriasis rosea by nested PCR. No DNA fragment of HHV-8 was found. Anti-HHV-8 IgM antibodies were also not detected by indirect immunofluorescence. Although 4 patients detected anti-HHV-8 IgG antibodies, their titers did not differ between the acute and late stages of pityriasis rosea. Therefore, it is believed that HHV-8 has nothing to do with pityriasis rosea. However, Prantsidis et al. detected 34 lesions of Kaposi’s sarcoma with typical pityriasis rosea by PCR. The results showed that 20.5% of patients had HHV-8 genome in their lesions. It is speculated that in some cases, HHV-8 may be associated with the onset of pityriasis rosea.

As the research progressed, it was discovered that pityriasis rosea may not be a single viral infection, it may be the synergy of two viruses or the interaction of multiple viruses. Watanabe et al. detected DNA of HHV6, HHV7, and cytomegalovirus in skin lesions, non-lesional skin, peripheral blood mononuclear cells, serum, and saliva of patients with pityriasis rosea. The results showed that the detection rate of HHV 7 DNA in different tissues was: skin lesion 93%, non-skin lesion 86%, saliva 100%, peripheral blood mononuclear cells 83%, serum sample 100%; HHV 6 DNA was skin Loss 86%, non-skin loss 79%, saliva 80%, peripheral blood mononuclear cells 83%, serum samples 88%. In contrast, DNA of HHV6, HHV7 was not detected in the serum and skin tissues of volunteers and 10 patients with psoriasis in these tissues. It is indicated that pityriasis rosea is associated with systemic infection of HHV6 and HHV7, whereas CMV does not play a role in pityriasis rosea. Since the virus is detected in saliva, it is speculated that the patient with pityriasis rosea may be reactivated instead of the primary infection because the salivary gland is a carrier of previous infections. In addition, the low level of virus in the lesions suggests that these viruses may not be directly infected with the skin, but rather a result of a systemic viral replication. The authors also speculate that the results of previous negative studies may be due to the fact that they did not use nested PCR and/or only extracted DNA from formaldehyde-fixed paraffin-embedded tissues. Another specimen of 21 patients with acute pityriasis rosea was observed by electron microscopy by Drago et al. In 15 specimens (71%), HHV particles were found in different morphogenesis periods. These particles were about 160-200 nm in diameter. There is a high electron density cylindrical core, a shell, a spike on the outer shell, and a layer of body between the shell and the outer shell. This further supports the role of HHV6 and HHV7 in pityriasis rosea. Broccolo et al. detected by real-time quantitative PCR that healthy volunteers and other inflammatory dermatological patients did not detect DAN of HHV6 and HHV7, while the detection rate of HHV6 DNA in patients with pityriasis rosea was 16%, and the detection rate of HHV7 DNA was 39. %, which provides further evidence for the role of HHV6 and HHV7 in pityriasis rosea. They point out that, as in previous studies, pityriasis rosea is the result of reactivation of the virus, not the primary infection. The study also noted that HHV7 reactivation may result in HHV6 reactivation, and vice versa. Drago et al. also found that in patients with pityriasis roseus with a course of more than 3 months, HHV-6 and/or HHV-7 had higher viral load and lasted longer than the common pityriasis rosea. It has also been found that viremia and oropharyngeal symptoms of children with pityriasis are associated with systemic reactivation of HHV-6 and/or HHV-7. In addition, Drago et al reported a case of chronic hepatitis C. When there was pityriasis rosea, the liver zymogram increased, and HCV-RNA, HHV-6 DNA and HHV-7 DNA were detected to be active and significantly elevated. After treatment, the liver zymogram returned to normal, HCV-RNA, HHV-7 DNA serum test was negative, the rash subsided, and the HHV-6 DNA serological test was significantly lower than before. Reactivation of HHV-6 is thought to result in activation of HHV-7 and HCV and induction of pityriasis rosea. Through the study of the above problems, it is believed that human herpesviruses 6 and 7 are the most likely causes of pityriasis rosea. Further research should aim to establish a clear relationship between them.

3. Viral infection participates in the treatment of pityriasis rosea

The impact of strategy Because of the self-limiting nature of PR, most patients only need to inform their natural course and follow up without taking active treatment. Ma-hajan et al. reviewed previous literatures that the treatment of pityriasis rosea is mainly divided into topical treatment and systemic treatment. Topical treatments include topical emollients, antihistamine ointments, corticosteroid ointments, systemic treatments including corticosteroids, antihistamines, and antibiotics. Viral drugs, antibiotics, phototherapy, etc. The literature pointed out that corticosteroids need to be used with caution, the recommended level is the lowest, because PR may be caused by viral infection, hormones can make the virus replicate. Macrolides and acyclovir are the most recommended, followed by phototherapy. The role of macrolides may be more due to their anti-inflammatory and immunomodulatory effects than antibacterial effects. In a comparative study of acyclovir and erythromycin in the treatment of pityriasis rosea, acyclovir was shown to be more effective than erythromycin. Ganguly’s randomized controlled double-blind clinical trial of oral acyclovir in the treatment of pityriasis rosea showed that the clinical efficacy of the acyclovir group was completely resolved in the acyclovir group compared with the placebo group at 7 and 14 days of treatment. The rates were 53.33% and 86.66%, respectively, compared with 10.00% and 33.33% in the placebo group, and the difference was statistically significant. Acyclovir is effective in treating pityriasis rosea. Chuh et al. conducted a systematic analysis of the literature and found that low-dose and high-dose acyclovir had a significant effect on reducing the itching symptoms of pityriasis rosea and accelerating the regression of rash, but had little to do with dose. Therefore, it is suggested that if the symptoms of pityriasis rosea are heavier, it is recommended to take a low dose (400mg 3 times/day) for 7 days. However, Singh et al. showed that acyclovir had no therapeutic effect on pityriasis rosea by a randomized controlled, triple-blind trial, but the patient’s observation period was between 26 and 33 days. Because pityriasis rosea usually takes place within 2 to 8 weeks of self-healing, Ma-hajan et al. recommend a 2-week test site to observe the therapeutic effect. For patients with pregnancy complicated with pityriasis rosea, Mahajan et al. According to the literature, the probability of abortion and premature delivery in patients with pregnancy and pityriasis rosea is increased, but there are no clinical reports, so the author believes that early pregnancy with pityriasis rose may be pregnancy. A warning of bad results. For gestation period, topical emollients and antihistamines may be considered, and systemic medication should be avoided as much as possible, and active follow-up should be taken. Ciccarese et al. pointed out that for general pityriasis rosea, the need for treatment still needs to be discussed, but for pregnancy with pityriasis rosea, especially within 15 weeks of pregnancy, pityriasis rosea may indicate intrauterine infection HHV-6/ 7, and may lead to adverse outcomes of premature birth or miscarriage. In this case, appropriate antiviral therapy can be considered.

4. Current problems

Pityriasis rosea is a self-limiting disease. From epidemiological analysis, the disease appears to be associated with pathogen infection, and the virus is most likely to be infected with HHV-6 and/or HHV-7. There is still a lack of evidence-based medical evidence for the treatment of pityriasis rosea, and early pregnancy with pityriasis rosea may be considered for antiviral therapy due to possible HHV infection and poor pregnancy outcomes. The cause and pathogenesis of true pityriasis rosea need further study.

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