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Current status and classification of viral skin diseases


The virus is the smallest pathogenic microorganism known to date, and can cause a variety of systemic infectious diseases, which are highly harmful. Viral skin disease refers to skin mucosal lesions caused by viral infection, such as herpes simplex, herpes zoster, chickenpox, sputum, etc. After the virus invades the human body, it has special tropism for various tissues, and has nerve and epidermal pro Addiction, some produce systemic multi-system clinical manifestations.

  1. The prevalence of viral skin diseases

1.1 Overview of virus infection

Viral infection is one of the main causes of human disease. The virus itself does not have a cellular structure, cannot be metabolized by itself, and can only be propagated in living host cells. At present, there are more than 500 common viruses. Some viral infections are limited to the skin mucosa and have tissue specificity of epithelial tissues, such as sputum caused by human papillomavirus, dysplasia of the epidermis, Bowenoid papulosis and infectious softness. Infectious soft palate caused by prions; some viral infections are mainly manifested by skin mucosa, and there are also systemic and multi-system symptoms such as chickenpox, smallpox, hand, foot and mouth disease and infectious erythema; some viral infections fall into the category of infectious diseases There are also characteristic skin manifestations, such as pediatric papular acromegaly caused by hepatitis B virus infection, and Kaposi’s sarcoma caused by human immunodeficiency virus infection. Among the newly discovered viral diseases, according to their history in the population, they can be divided into three categories: 1 The disease itself has long been recognized, but it is not considered to be a viral disease, such as baby rose rash and pityriasis rosea. Human herpesvirus type 6,7 infection is associated with infectious erythema associated with human parvovirus B19. 2 The disease may already exist in the population, but it is only recognized after the virus is discovered, such as hepatitis C and hepatitis E. It has been found that as many as 40% to 74% of hepatitis C patients have at least one disease during the onset. Extrahepatic manifestations. 3 The disease may not exist in the population in the past, it is indeed a new viral disease, such as AIDS, Ebola virus. Advances in modern transportation have caused some regional diseases to break through the boundaries and spread to distant areas with similar natural conditions. Bad behaviors such as sexual disorder and intravenous drug use can lead to the spread of sexually transmitted diseases, AIDS, viral hepatitis and the like. In addition, long-term use of immunosuppressive drugs after organ transplantation is also likely to cause infection by cytomegalovirus (CMV), varicella-zoster virus (VZV), hepatitis B virus (HBV), and hepatitis C virus (HCV). The use of iatrogenic infections, such as blood transfusions and blood products, has led to an increase in blood-borne viral diseases. These factors contribute to the occurrence and spread of viral skin diseases. In recent years, people have also gained a new understanding of the carcinogenicity of the virus. Many tumor diseases have been found to be associated with viral infections, especially DNA viruses, such as nasopharyngeal and EB viruses, cervical and human papillomaviruses, cytomegalovirus, Kaposi’s sarcoma and human herpesvirus type 8, hepatocellular carcinoma and Hepatitis B virus, etc. RNA viruses such as hepatitis C virus are also closely related to the development of liver cancer.

1.2 Epidemic status of human herpesvirus

Herpes virus is a common pathogen in viral skin diseases, and there are 8 common viruses in the human herpesvirus family. Herpes simplex virus (HSV)-2 infection is highly prevalent in many parts of the world. The world’s first HSV-2 infection report shows that 536 million people in the 15-49 age group are infected with HSV-2, and more than 23 million infections are added each year. Case. There are differences in the prevalence among countries with different levels of development. The infection rate in developing countries is much higher than in developed countries, and the female infection rate is higher than that of males. Analysis of the infected population found that HSV-2 infection was mainly caused by extramarital sex, mainly farmers and workers with lower education level. Herpes zoster has a high incidence, and severe cases can cause unbearable neuralgia, which cannot be ignored in the study of viral skin diseases. The incidence of herpes zoster in the United States is 3.2/1000 to 4.2 / 1000 person-years, and the incidence rate of people aged 60 years and over is as high as 10 / 1 000 person-years. Age, gender, season and geographical factors, VZV infection history, VZV exposure History, varicella vaccination history, immune function, etc. are all risk factors. The research on herpes virus mainly focuses on its immune response with the body and vaccine research. Herpes simplex virus can be latent in the body for a long time and cause periodic recurrence. The development of HSV-2 vaccines has been greatly improved in terms of safety and efficacy from inactivated vaccines to DNA vaccines, but it has not yet been applied in clinical practice.

1.3 Epidemic status of human papillomavirus

Wart is a benign skin disease caused by human papillomavirus infection of the skin mucosa, mostly caused by HPV type 1,2,4 infection, and the most common cause of hand, foot and vulgaris is HPV2 type; condyloma acuminata is mostly caused by HPV6,11 Type caused. The global incidence of condyloma acuminata between 2001 and 2012 averaged 194/100,000. Chen Sihua et al analyzed 2094 cases of condyloma acuminata, and found that the clinical incidence of condyloma acuminata increased year by year, 20 to 50 years old is a high incidence age group, and male, age >50 years, disease course >3 months, lesions located in the cervix and anal canal Internal and genital herpes, combined urinary tract infection, and HIV positive are risk factors for recurrence. Reports show that at least 80% of sexually active people are infected with one or more types of HPV, about 15% are subclinical or latent, and only 1% have typical clinical manifestations.

1.4 The prevalence of AIDS

AIDS, also known as acquired immunodeficiency syndrome, is a series of symptoms induced by human immunodeficiency virus infection that ultimately leads to death from sexually transmitted diseases. Because of its rapid spread and high mortality, and there are still no effective cures and vaccines, it has become a global public health problem. According to the AIDS case report, as of August 2016, the country reported 645,541 HIV-infected/AIDS patients and reported 198,523 deaths. Among them, high-risk sexual behaviors such as not using condoms, multiple sexual behaviors, multiple sexual partners, and other sexually transmitted diseases are all factors that promote the spread of AIDS. In the investigation and analysis, it was found that the overall domestic AIDS epidemic was low, but the epidemic situation was serious in some areas, and the number of infections and patients continued to grow slowly year by year. The first sexual behavior age of high-risk groups tends to be younger, male homosexuality. The crowd became a bridge for HIV transmission. 2 Classification of viral skin diseases As many as 500 kinds of viruses cause infectious skin diseases, and their classification also has various standards. The simple classification principles mainly include:①Type and structure of nucleic acid (DNA, RNA, double-stranded, single-stranded, circular, linear, segmented);②The shape and size of the virion;③Morphological structure of virion (symmetry of capsid, presence or absence of envelope);④Sensitivity to lipid solvents, etc. According to the rash after infection, it can be divided into:1)Blister type, such as herpes simplex, herpes zoster, chickenpox, smallpox, etc.;2)Rash type, such as measles, rubella, etc.;3)New biotypes, such as common warts, infectious soft palate, etc. According to the chemical composition of the nucleic acid, it can be divided into two major categories: DNA virus and RNA virus, and different sub-classes according to the size and shape of the virus, the sub-structure and antigenicity of the virus particles, as shown in Table 1.

Table 1 Common viral skin disease classification

Virus classification     Related diseases
DNA virus Herpesviridae Herpes simplex virus Herpes simplex, kaposi varicella-like rash, encephalitis
    Chickenpox-zoster virus Chickenpox, herpes zoster
    Cytomegalovirus Cytomegalovirus infection, giant cell inclusion disease
    EB virus Infectious mononucleosis
    Human herpesvirus type 6 Children’s acute rash, baby rose rash
    Human herpesvirus 7 Plaque-like rash
    Human herpesvirus type 8 Kaposi sarcoma
    B virus B virus
  Poxvirus Smallpox virus Smallpox, vaccination, vaccinia, vaccinia-like eczema
    Vaccinia virus Milking man nodules, sheep pox
    Infectious soft prion Contagious soft palate
    Monkey variola virus Monkey variola virus disease, Yaha monkey virus disease
  Papilloma multifocal vacuolid virus   Common warts, flat warts, warts, condyloma acuminata, sputum epidermal dysplasia, Bowenoid papulosis, oral focal epithelial hyperplasia
  Hepatitis virus   Pediatric papular dermatitis, hepatitis B antigenemia
RNA virus Small RNA virus Coxsackie virus Hand, foot and mouth disease, foot and mouth disease, coxsack eczema, coxsackie virus rash
    Echovirus Echo virus rash, Boston rash
    Arbovirus Dengue fever, viral hemorrhagic fever
    Adenovirus Adenovirus rash
  Paramyxoviridae Measles virus Measles, atypical measles syndrome
    Respiratory fusion virus Respiratory fusion virus infection
    Rubella virus Rubella, rubella syndrome
  Retroviral   AIDS
May be a viral infection of the skin disease     Infectious erythema, infantile acute rash, Kawasaki disease


  1. Human herpesvirus skin disease

2.1 Herpesvirus is a group of enveloped DNA viruses with skin and neurotropic properties. It is divided into three subgroups: α, β and γ. There are 8 types that can infect humans. Viral infection of host cells can be manifested in a variety of infection types, such as dominant infections, latent infections, integrated infections, congenital infections, and the like.

2.1.1 Herpes simplex virus infection

Herpes simplex virus (HSV) type 1 initial infection occurs in children, mainly causing skin mucosa and brain infections other than genitals. Type 2 primary infections are mainly found in young adults or adults. They are transmitted through close contact or vertical infection, mainly causing genital mutilation. Site or neonatal infection. After the virus invades the skin mucosa, it forms a primary infection in the local proliferation, and the long-term latent lurks in the ganglia that follow the nerve endings to the innervation nerve. When the virus is stimulated by factors such as decreased resistance, the virus can be activated and migrated. Epithelial tissue distributed to the nerve endings. The mechanism of latent infection and recurrence may be related to immune escape after virus infection, inhibition of early immediate protein expression by viral latent transcript (LAT) gene, regulation of viral genome and host cell, viral genome coding. MicroRNA-mediated regulation is related to the sequence of CTCF-specific binding. Clinical manifestations of herpetic gingivitis, neonatal herpes simplex, herpetic eczema, vaccination herpes, herpetic keratoconjunctivitis, genital herpes and recurrent herpes, mainly characterized by erythema, clustered small papules and small blisters, broken After the ulceration, a superficial ulcer is formed.

2.1.2 Varicella-zoster virus infection

Varicella-zoster virus (VZV) or human herpesvirus type 3 (HHV-3) has only one serotype and is the only host of VZV. The virus enters the bloodstream through the respiratory mucosa to form viremia, which causes varicella or invisible infection. The posterior virus is lurking in the posterior root ganglia or cranial nerve sensory ganglia of the spinal cord. When the body is subjected to certain stimuli such as trauma, fatigue, malignant tumor, and weakness Etc., the latent virus is activated to replicate along the axons down to the inner region of the dominating region, and the affected nerves are inflammatory and necrotic. The clinical manifestations are clustered blisters distributed along the unilateral side of the nerve, accompanied by neuralgia.

2.1.3 Human herpesvirus infection

Human herpesvirus (HHV)-4, EBV (EBV), is the causative agent of infectious mononucleosis and is associated with malignant lymphoma and nasopharyngeal carcinoma by adsorbing CD21 molecules on the surface of human B lymphocytes. Infected B cells, often manifested as extreme fatigue, pharyngitis or tonsillitis, large cervical lymph nodes, large liver and splenomegaly. Cytomegalovirus (CMV) is the causative agent of giant cell inclusion disease and is named for the enlargement of infected cells with large intranuclear inclusions. CMV is mostly latent infection, which can be activated by factors such as pregnancy, multiple blood transfusions or organ transplantation, and can also cause dominant infection. The virus can also occur vertically, which is harmful to the fetus. It is one of the important pathogens causing congenital malformation, and also an important cause of organ transplantation, tumor and AIDS death. The morphological structure of human herpesvirus type 6 (HHV-6) is similar to that of other herpes viruses, while molecular virology and immunology studies show differences. The primary infection can cause papules or baby rose rash in children, and then lurk in the human body for a long time. Blood lymphocytes and parotid glands may be important parts of latency. When the body’s immune function is low or an immunosuppressive agent is used, latent HHV-6 is activated, causing febrile disease, interstitial pneumonia, myelosuppression and bone marrow failure in organ transplant patients, and may also work with HHV-4. Causes chronic spontaneous urticaria. Human herpesvirus type 7 (HHV-7) is an unexpected finding in the study of AIDS. Like HHV-6, it is latent in the human body after the primary infection, but its latent part is not fully understood. Human herpesvirus type 8 (HHV-8), also known as Kaposi’s sarcoma-associated herpesvirus (KSHV), detects DNA in serum, plasma, and peripheral blood leukocytes of patients with Kaposi’s sarcoma. Studies have shown that HHV-8 may be involved in the onset of Kaposi’s sarcoma and proliferative diseases. Herpesviruses including EB, HHV-6, HHV-7, and HHV-8 may contribute to HIV infection and progression, and inhibition of HSV may reduce HIV-1 infectivity and delay its progression.

2.2 Poxvirus infectious skin disease

Poxvirus is a very large and unique ds DNA virus, which looks like a brick and has a composite symmetry of the nucleocapsid. The replication of all nucleic acids of the poxvirus is completed in the cytoplasm of the infected cells, and all the polymerases, ligases, etc. of the cells are located in the nucleus and cannot be utilized by the virus. Therefore, poxvirus viruses carry transcriptase in vivo and can transcribe and synthesize all the enzymes required for viral replication. The poxvirus can also directly synthesize its own envelope, rather than just modifying the host cell membrane. Poxvirus infection can form inclusion bodies in the cytoplasm of the host cell. Smallpox virus, vaccinia virus, para-vaccinia virus and infectious soft prion are all poxviruses. The wild strain of variola virus has been extinct since 1977, and vaccinia virus is a vaccine against variola virus. Infectious soft prion is another poxvirus. Currently, type 4 and several subtypes are found, and close contact between the skin is the main mode of transmission. The clinical manifestation is gray or pearl color plate-shaped papules with a diameter of about 3 to 5 mm. The surface has waxy luster. The center has umbilical fossa, which can extrude milky white cheese-like substance, which is a large eosinophilic substance in the cytoplasm of infected cells. Containing Hugh, called soft corpus callosum.

2.3 Human papillomavirus skin disease

Human papillomavirus is a group of small, non-enveloped DNA viruses that induce the production of tendons and papillomas in the skin and mucous membranes of humans and a variety of advanced vertebrates such as rabbits, cattle and dogs. According to its morphology and pathogenic conditions, the virus is divided into three types: human papillomavirus, polyomavirus, and vacuolar virus. Among them, human papillomavirus (HPV) has become an important pathogen that seriously endangers human health. More than 200 different HPV types, subtypes and mutant strains have been found to infect skin basal epithelial cells or tissue mucosa, which are classified into skin type and mucosa type. HPV skin type generally invades the skin of the hands and feet to cause common warts; mucosal type mainly infects the mouth, throat, respiratory tract or genital covering epithelium. HPV enters the cell through micro-disruption of skin mucosa to replicate and proliferate, leading to abnormal differentiation and proliferation of epithelial cells, causing epithelial benign neoplasms. Unlike the invasion of the general virus, HPV breaks down into basal cells and decomposes into individual components. After the genome is replicated, the protein is expressed and then reassembled into new particles, interfering with the expression of cytokeratin polypeptide, causing abnormal keratinization of epithelial cells. Studies have also shown that HPV may cause abnormal cell proliferation in the regulation of the cell cycle. In the clinical manifestations of common warts, flat warts, warts and condyloma acuminata, the typical skin lesions are yellow or brown pimples of yellow bean size, the surface is rough or smooth, and autologous inoculation can be formed after scratching.

2.4 Hepatitis virus-associated skin disease

Recent studies have found that many skin diseases may be associated with hepatitis C virus (HCV) infection, including cryoglobulinemia, nodular polyarteritis, delayed porphyria, lichen planus, urticaria, necrosis Sexual erythema, vitiligo, polymorphous erythema, pruritus and acquired bullous epidermolysis. The current replication of HCV in the skin or mucous membranes has not been clearly demonstrated. Pediatric papillary dermatitis is also considered to be a skin manifestation of hepatitis B virus infection, which is associated with the deposition of antigen-antibody complexes of hepatitis B virus.

2.5 Small RNA virus infectious disease

Coxsackie virus (Cox V) is classified into the microRNA virus family and the enterovirus genus. It is divided into groups A and B due to its different pathogenicity to suckling mice, which can cause Coxsack eczema. Echovirus has 38 serotypes that can cause a variety of serious clinical syndromes, such as aseptic meningitis, multiple radiculitis, myocarditis, epidemic myalgia, respiratory or rash disease. Studies have shown that Echoviruses E11 and E30 have high genetic variation and their 1/3 nucleotides are variable.

2.6 Paramyxovirus infectious disease

Measles is a highly contagious acute infectious disease characterized by fever, conjunctivitis, upper respiratory tract infection, Koplik plaque and systemic red maculopapular rash. It is highly contagious, from the fifth day after infection to the second after rash. It is contagious for 5 days, and it can get long-lasting immunity. Two to four days after infection with measles virus, the virus replicates in the upper respiratory tract and spreads to the local lymphoid tissue, which is carried by the pulmonary macrophages into the blood and replicated in macrophages and lymphocytes to cause a second virus. The blood is spread to the whole body reticuloendothelial system and then spreads to the whole body epithelial tissue with prodromal symptoms. On the 13th to 16th day of infection, a wide-ranging skin rash appeared, and with the formation of a cellular immune response, specific antibodies appeared to terminate the replication of the virus. Rubella virus, also known as German measles, is a benign respiratory rash infection that has infectious diseases from 5 days before the rash to 2 days after the rash, showing fever, rash and superficial lymph nodes. Intrauterine infection can occur through the placenta, if the infection within 3 months of pregnancy can cause congenital malformations. Respiratory syncytial virus often causes lower respiratory tract infections in clinical practice, and a few cases show viral rash. Its virulence structure and maturation process are similar to other paramyxoviruses, and a special structural protein M2 plays a role in transcription and replication of the virus. Important role.

2.7 Arbovirus infectious disease

Arbovirus is a virus that spreads between vertebrate and bloodthirsty arthropod hosts. There are more than 250 kinds of viruses that can infect at least 80 species, including the Flaviviridae (B encephalitis virus, yellow fever). Disease virus, forest encephalitis virus), togaviridae (eastern equine encephalitis virus, western equine encephalitis virus, Venezuelan equine encephalitis virus) and Bunia virus family (hantan virus, Xinjiang hemorrhagic fever virus). The new arbovirus, Nanding virus, first discovered in Culex pipiens in 2011, may be associated with the development of acute encephalitis syndrome.

2.8 Parvovirus infectious disease parvovirus

B19 is a parvovirus known to be pathogenic to humans. It can replicate in human red blood cells and proliferate in skin cells, causing epidermal cell edema, dermal papillary vasodilatation, endothelial cell swelling and bleeding, causing infectious erythema and purpura. Etc., with facial, hip and limb-specific erythema as clinical features, there is a high infection rate and incidence in children in China.

2.9 Human acquired immunodeficiency syndrome

Human immunodeficiency virus (HIV), commonly known as HIV, can cause human acquired immunodeficiency syndrome. HIV belongs to the genus of primate immunodeficiency viruses in the retrovirus family of lentiviruses. HIV has a unique viral particle structure, its structural protein is mainly encoded by four groups of genes, the gag gene encodes the core protein of the virus, the pol gene encodes the enzyme required for viral replication, and the sequence beginning in the overlapping region of the pol and gag genes is called The por gene, which encodes the protease p22, plays a major role in the cleavage of the HIV protein precursor to form a terminal mature protein, which encodes the HIV envelope glycoprotein precursor gp160. When HIV enters the human body, its envelope glycoprotein gp120 infects T4 lymphocytes, infects other types of cells such as B lymphocytes, monocytes and different cell lines, and integrates its own DNA into the host cell DNA by reverse transcription in the target cell nucleus. Medium, or reassembled into new viral particles, releasing new HIV to kill cells, or entering the incubation period for life to be carried in infected cells and their progeny cells, once activated, mass reproduction. HIV is constantly killing host cells during reproduction, reducing T lymphocytes in the body, and other immune cells are also damaged, resulting in defects in immune function, leading to opportunistic infections and tumors in the body. Nowadays, the disease has swept the world rapidly, becoming the world’s most serious viral disease that endangers human health and life.


  1. Conclusion of viral skin diseases

With the development of medical technology, the improvement of human living standards, the transformation of lifestyles and the increase of the aging population, the disease spectrum will undergo significant changes. However, molecular virological studies have shown that viruses have strong ability to evolve, adapt, and develop resistance. New viruses, especially those that are very lethal, are constantly being discovered. Old viral diseases are ups and downs, potential threats are serious, and the relationship between viral infections and clinical diseases is receiving increasing attention. Therefore, in the new century, viral diseases are still an important issue threatening human health. It is necessary to actively strengthen research and continue to find new prevention and control measures to protect human health.

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