Mumps Virus- An Overview

Mumps virus is a member of the family Paramyxoviridae, which includes other human pathogens such as measles, respiratory syncytial virus, and parainfluenza viruses. Mumps virus causes an acute infection of the salivary glands and other organs, and can lead to complications such as meningitis, orchitis, oophoritis, and pancreatitis.

The structure of mumps virus is similar to other paramyxoviruses. It consists of an outer envelope that surrounds an inner helical nucleocapsid. The envelope is derived from the host cell membrane and contains two types of glycoproteins: hemagglutinin-neuraminidase (HN) and fusion (F) protein. The HN protein binds to sialic acid receptors on the surface of host cells and facilitates viral attachment and entry. The F protein mediates the fusion of the viral envelope with the cell membrane and allows the release of the nucleocapsid into the cytoplasm. The nucleocapsid is composed of a single-stranded RNA genome that is associated with three proteins: nucleoprotein (NP), phosphoprotein (P), and large (L) protein. The NP protein forms a helical structure around the RNA and protects it from degradation. The P protein acts as a cofactor for the L protein, which is the viral RNA polymerase that transcribes and replicates the viral genome.

The mumps virus genome is about 15.3 kilobases long and has a negative polarity, meaning that it is complementary to the mRNA that is produced from it. The genome contains six genes that encode for six structural proteins: NP, P, M (matrix), F, SH (small hydrophobic), and HN. The genes are arranged in a fixed order from 3` to 5` end: 3`-NP-P-M-F-SH-HN-L-5`. The genome also has a non-coding leader sequence at the 3` end and a trailer sequence at the 5` end that are involved in transcription and replication.

The structure of mumps virus determines its infectivity, antigenicity, and pathogenicity. The envelope glycoproteins are responsible for binding to host cells and initiating infection. They are also the main targets of neutralizing antibodies that can prevent infection or limit its spread. The nucleocapsid proteins are involved in viral replication and transcription, and also elicit cellular immune responses that can clear the infection or cause tissue damage. Understanding the structure of mumps virus can help in developing effective vaccines and antiviral drugs against this important human pathogen.

The mumps virus (MuV) is a negative-sense, single-stranded RNA virus that belongs to the genus Orthorubulavirus in the family Paramyxoviridae. Its genome is about 15.3 kilobases (kb) long and contains seven genes that encode nine proteins. The genome is encased by a nucleocapsid protein (N) that forms a helical structure inside the viral envelope.

The gene order of MuV is 3’-N-P-M-F-SH-HN-L-5’, where N is the nucleocapsid protein, P is the phosphoprotein that forms the RNA-dependent RNA polymerase (RdRp) with the large protein (L), M is the matrix protein that lines the inner surface of the envelope, F is the fusion protein that mediates membrane fusion, SH is the small hydrophobic protein that inhibits host cell apoptosis, HN is the hemagglutinin-neuraminidase protein that binds to sialic acid receptors on host cells, and L is the large protein that acts as the RdRp .

The genome has a non-transcribed leader sequence of 55 nucleotides and a trailing sequence of 24 nucleotides at the 3’ and 5’ ends, respectively. These sequences have complementary regions that allow the genome to form a circular structure. The genome also has conserved gene start and gene end sequences that flank each gene and regulate transcription and replication.

The MuV genome serves as both a template for mRNA transcription and a template for genome replication. The RdRp transcribes each gene into a capped and polyadenylated mRNA by recognizing the gene start and gene end signals. The RdRp also replicates the genome by synthesizing a positive-sense antigenome from the negative-sense genome, and then synthesizing a negative-sense genome from the positive-sense antigenome.

The MuV genome is highly variable among different strains and isolates. Based on nucleotide sequence analysis of the SH gene, 12 genotypes of MuV have been identified (A to N, excluding E and M) that differ in their geographic distribution and epidemiology. Whole genome sequencing can provide more information on the genetic diversity and evolution of MuV strains and help in outbreak investigation and vaccine development.

Mumps is a contagious viral infection that affects the salivary glands and other organs. It is transmitted by respiratory droplets or direct contact with saliva or mucus of an infected person. Mumps can also spread through fomites, such as utensils, cups, or toys that have been contaminated with the virus.

Mumps occurs worldwide, but the incidence and severity vary depending on the level of vaccination coverage, population immunity, and environmental factors. Mumps is more common in temperate regions than in tropical regions, and it usually peaks in winter and spring. Mumps affects mainly children and adolescents, but adults can also get infected. The average incubation period is 16 to 18 days, but it can range from 12 to 25 days.

Before the introduction of the mumps vaccine in the 1960s, mumps was a common childhood disease that caused outbreaks in schools, camps, and military barracks. The vaccine has reduced the number of cases and complications by more than 99% in countries with high immunization rates. However, mumps outbreaks still occur sporadically in some regions, especially among unvaccinated or partially vaccinated populations, or in settings where close contact facilitates transmission.

According to the World Health Organization (WHO), there were about 1.2 million reported cases of mumps globally in 2019, with the highest numbers in Africa and Europe. However, many cases are not reported or diagnosed, so the actual burden of disease may be higher. The WHO estimates that mumps causes about 60,000 deaths per year worldwide, mostly due to encephalitis.

The most effective way to prevent mumps is to get vaccinated with two doses of the measles-mumps-rubella (MMR) vaccine or the measles-mumps-rubella-varicella (MMRV) vaccine. The first dose is usually given at 12 to 15 months of age, and the second dose at 4 to 6 years of age. The vaccine provides about 88% protection against mumps infection. However, some people may still get mumps even if they are fully vaccinated, especially if they are exposed to a large amount of virus or if their immunity wanes over time.

Other preventive measures include avoiding contact with people who have mumps, covering the mouth and nose when coughing or sneezing, washing hands frequently with soap and water or using alcohol-based hand sanitizer, and disinfecting surfaces and objects that may be contaminated with the virus.

Mumps virus replicates in the cytoplasm of infected cells. The replication process can be divided into four main steps: attachment, entry, transcription and replication, and assembly and release.

Attachment

The first step of mumps virus replication is the attachment of the virus to the host cell surface. The virus uses its hemagglutinin-neuraminidase (HN) protein to bind to sialic acid residues on cellular glycoproteins or glycolipids. The HN protein also has neuraminidase activity, which cleaves sialic acid from the receptors and prevents viral aggregation.

Entry

The second step of mumps virus replication is the entry of the virus into the host cell. The virus uses its fusion (F) protein to mediate the fusion of the viral envelope with the plasma membrane of the cell. This allows the release of the nucleocapsid, which contains the viral RNA and associated proteins, into the cytoplasm. The F protein is activated by a low pH environment or by cleavage by cellular proteases.

Transcription and Replication

The third step of mumps virus replication is the transcription and replication of the viral RNA. The nucleocapsid acts as a template for the synthesis of viral mRNA and genomic RNA by the viral RNA polymerase (L protein). The viral mRNA is capped and polyadenylated by the viral phosphoprotein (P protein), which also facilitates RNA synthesis. The viral mRNA is translated into viral proteins by the host cell ribosomes. The viral proteins include structural proteins (N, P, L, M, F, HN) and a nonstructural protein (SH).

The viral RNA polymerase switches from transcription to replication when the concentration of N protein reaches a critical level. The N protein binds to the nascent positive-sense antigenome intermediates and prevents their polyadenylation and termination. The antigenome serves as a template for the synthesis of negative-sense genomic RNA. The genomic RNA associates with N, P, and L proteins to form new nucleocapsids.

Assembly and Release

The final step of mumps virus replication is the assembly and release of new virions. The nucleocapsids interact with the matrix (M) protein under the plasma membrane and bud out via the ESCRT complex, acquiring an envelope with F and HN proteins. The new virions are released from the cell and can infect other cells or spread through saliva or urine.

Mumps virus is transmitted by respiratory droplets and infects the epithelial cells of the upper respiratory tract. The virus then replicates in the nasopharynx and regional lymph nodes, where it induces an innate immune response and interferon production. Within a few days, the virus enters the bloodstream and disseminates to various organs and tissues, such as the salivary glands, the central nervous system, the testes, the ovaries, the pancreas, and the thyroid gland. The virus has a tropism for glandular epithelial cells and neurons, where it causes inflammation, edema, and tissue damage. The pathogenesis of mumps virus is influenced by several factors, such as the viral strain, the host immune status, the age of infection, and the presence of underlying conditions .

The most common and characteristic manifestation of mumps virus infection is parotitis, which occurs in about 50% of symptomatic cases. Parotitis is caused by viral invasion of the ductal epithelium of the parotid glands, resulting in intracytoplasmic inclusions, viral antigen expression, cell desquamation, and obstruction of saliva flow. The inflammation and swelling of the parotid glands cause pain, fever, headache, loss of appetite, and difficulty in chewing or swallowing.

Another frequent complication of mumps virus infection is orchitis, which affects about 20-50% of postpubertal males. Orchitis is caused by viral infection of the seminiferous tubules and interstitial cells of the testes, leading to inflammation, hemorrhage, necrosis, and atrophy. Orchitis can cause severe pain, swelling, tenderness, and redness of the scrotum. Orchitis can also impair spermatogenesis and result in subfertility or sterility in rare cases .

Mumps virus can also infect the central nervous system and cause meningitis or encephalitis in 10-30% of cases. Mumps virus enters the central nervous system through the blood-brain barrier or via retrograde axonal transport from peripheral nerves. The virus preferentially infects neurons and glial cells in various regions of the brain and spinal cord, causing inflammation, demyelination, neuronal death, and neurological dysfunction. Mumps meningitis is characterized by headache, stiff neck, photophobia, nausea, vomiting, and altered mental status. Mumps encephalitis can present with seizures, focal neurological deficits, cranial nerve palsies, deafness, coma, or death .

Other less common manifestations of mumps virus infection include oophoritis (inflammation of the ovaries), pancreatitis (inflammation of the pancreas), mastitis (inflammation of the breast), thyroiditis (inflammation of the thyroid gland), myocarditis (inflammation of the heart muscle), arthritis (inflammation of the joints), nephritis (inflammation of the kidneys), hepatitis (inflammation of the liver), and keratoconjunctivitis (inflammation of the cornea and conjunctiva). These conditions are usually mild and self-limiting .

Mumps virus infection during pregnancy can cause fetal wastage or congenital malformations due to placental infection or transplacental transmission. Mumps virus can also be transmitted through breast milk or semen .

The clinical manifestations of mumps virus infection vary depending on the age, immune status, and organ involvement of the patient. The most common and characteristic symptom of mumps is parotitis, or inflammation and swelling of the parotid glands, which are located on both sides of the face below the ears. Parotitis occurs in about 50% of symptomatic cases and usually develops 16 to 18 days after exposure to the virus. Parotitis may be unilateral or bilateral, and may cause pain, tenderness, fever, headache, and difficulty in chewing or swallowing. Parotitis usually lasts for 7 to 10 days and resolves spontaneously.

Mumps virus can also infect other salivary glands, such as the submandibular and sublingual glands, causing similar symptoms. In addition, mumps virus can spread to various organs and tissues through the bloodstream or lymphatic system, causing complications such as:

• Meningitis. This is the most common complication of mumps virus infection, affecting 10 to 30% of cases. Meningitis is an inflammation of the membranes that cover the brain and spinal cord. Mumps meningitis usually occurs 5 to 7 days after the onset of parotitis, but may also occur without parotitis or before it. Mumps meningitis causes symptoms such as fever, headache, stiff neck, nausea, vomiting, and sensitivity to light. Mumps meningitis is usually mild and self-limiting, and rarely causes permanent neurological damage or death.
• Encephalitis. This is a rare but serious complication of mumps virus infection, affecting less than 1% of cases. Encephalitis is an inflammation of the brain tissue that can cause severe neurological symptoms such as confusion, seizures, coma, and paralysis. Encephalitis may occur at any time during the course of mumps infection, but is more common in adults than in children. Encephalitis may result in permanent disability or death.
• Orchitis. This is a common complication of mumps virus infection in males who have reached puberty, affecting 20 to 50% of cases. Orchitis is an inflammation of one or both testicles that can cause pain, swelling, redness, and fever. Orchitis usually occurs 4 to 8 days after the onset of parotitis, but may also occur without parotitis or before it. Orchitis may lead to testicular atrophy (shrinkage) or impaired fertility (reduced sperm production), but sterility is rare.
• Oophoritis. This is a rare complication of mumps virus infection in females who have reached puberty, affecting about 5% of cases. Oophoritis is an inflammation of one or both ovaries that can cause lower abdominal pain, fever, and vaginal discharge. Oophoritis usually occurs during or after the resolution of parotitis. Oophoritis may lead to ovarian cysts or impaired fertility (reduced egg production), but sterility is rare.
• Pancreatitis. This is a rare complication of mumps virus infection, affecting about 4% of cases. Pancreatitis is an inflammation of the pancreas that can cause upper abdominal pain, nausea, vomiting, and elevated blood sugar levels. Pancreatitis usually occurs during or after the resolution of parotitis. Pancreatitis may lead to hemorrhage (bleeding), necrosis (tissue death), or diabetes mellitus (chronic high blood sugar).
• Deafness. This is a rare but serious complication of mumps virus infection, affecting about five in 100,000 cases. Deafness is a loss of hearing that can be partial or complete, unilateral or bilateral. Deafness may occur at any time during the course of mumps infection, but is more common in children than in adults. Deafness may be temporary or permanent.
• Miscarriage. This is a rare complication of mumps virus infection in pregnant women who contract the virus during the first trimester (first three months) of pregnancy. Miscarriage is a loss of pregnancy that can be caused by blood-borne infection of the placenta or direct infection of the fetal tissues by mumps virus. Miscarriage may result in bleeding, cramping, and expulsion of fetal tissue.

Mumps virus infection can also cause other less common complications such as hepatitis (inflammation of the liver), myocarditis (inflammation of the heart muscle), nephritis (inflammation of the kidneys), arthritis (inflammation of the joints), thyroiditis (inflammation of the thyroid gland), mastitis (inflammation of the breast tissue), prostatitis (inflammation of the prostate gland), epididymitis (inflammation of the epididymis), and keratoconjunctivitis sicca (dryness and irritation of the eyes).

Most patients with mumps virus infection recover completely without any long-term consequences. However, some patients may experience chronic or recurrent symptoms such as fatigue, depression, anxiety, memory loss, cognitive impairment, or chronic pain.

The overall mortality rate for mumps virus infection is low (one death per 10,000 cases in the United States), mostly caused by encephalitis or other complications involving vital organs.

The incidence and severity of mumps virus infection and its complications have declined significantly since the introduction of the live-attenuated mumps vaccine in 1967. However, outbreaks still occur occasionally among unvaccinated or partially vaccinated populations or among vaccinated individuals with waning immunity.

Therefore, prevention through vaccination remains the best strategy to protect against mumps virus infection and its complications.

The laboratory diagnosis of mumps virus infection can be done by various methods, such as virus isolation, nucleic acid detection, and serology. These methods can help confirm the clinical diagnosis, identify the virus strain, and monitor the immune status of the patient.

Virus isolation

Virus isolation is the gold standard for mumps virus diagnosis. It involves culturing the virus from clinical specimens, such as saliva, urine, cerebrospinal fluid (CSF), or tissue biopsies. The specimens should be collected as early as possible after the onset of symptoms and transported under cold conditions to prevent viral degradation.

The most commonly used cell culture system for mumps virus isolation is monkey kidney cells, either primary or continuous lines. Other cell lines, such as Vero, LLC-MK2, or B95a, can also be used. The inoculated cells are incubated at 35–37°C and observed daily for cytopathic effects (CPE), such as syncytia formation or cell lysis. The CPE may take up to 10 days to appear, depending on the viral load and strain.

To confirm the presence of mumps virus in the culture, hemadsorption techniques can be applied to detect the viral hemagglutinin-neuraminidase (HN) protein on the cell surface. Alternatively, immunofluorescence assays (IFA) can be performed using mumps-specific antibodies to stain the viral antigens in the infected cells. These methods can also help differentiate mumps virus from other paramyxoviruses that may cause similar CPE.

Virus isolation is a sensitive and specific method for mumps virus diagnosis, but it is also time-consuming, labor-intensive, and requires biosafety level 2 facilities and expertise.

Nucleic acid detection

Nucleic acid detection is a rapid and sensitive method for mumps virus diagnosis. It involves amplifying and detecting the viral RNA from clinical specimens using reverse transcription polymerase chain reaction (RT-PCR) or other molecular techniques.

The most commonly used target for RT-PCR is the small hydrophobic (SH) gene of mumps virus, which is highly conserved among different strains. Other targets, such as the nucleoprotein (NP), fusion (F), or HN genes, can also be used. The primers and probes for RT-PCR should be designed to match the circulating strains of mumps virus in the region.

The specimens for RT-PCR should be collected as early as possible after the onset of symptoms and stored at -70°C until testing. The extraction and amplification of viral RNA should be performed under strict quality control measures to avoid contamination and false-positive results.

RT-PCR can detect mumps virus in many clinical samples that have negative results in virus isolation attempts. It can also identify the virus strain and provide useful information for epidemiological studies and outbreak investigations. However, RT-PCR requires specialized equipment and trained personnel and may not be widely available in resource-limited settings.

Serology

Serology is a simple and convenient method for mumps virus diagnosis. It involves measuring the antibody response to mumps virus infection in serum samples using enzyme-linked immunosorbent assay (ELISA) or hemagglutination inhibition (HI) test.

The antibodies against mumps virus can be classified into two types: IgM and IgG. IgM antibodies are produced early in the infection and indicate recent or acute infection. IgG antibodies are produced later in the infection and indicate past infection or immunity.

The serum samples for serology should be collected in two phases: acute phase (within 7 days of symptom onset) and convalescent phase (2–4 weeks later). A fourfold or greater rise in antibody titer between the two phases is considered diagnostic of mumps virus infection. Alternatively, a single serum sample with a high IgM titer (>1:160) or a low IgG avidity index (<30%) can also suggest recent infection.

Serology is a useful method for mumps virus diagnosis when virus isolation or RT-PCR are not feasible or available. However, serology has some limitations, such as cross-reactivity with other paramyxoviruses, interference by vaccination or passive immunity, and delay in antibody production in some cases. Therefore, serology results should be interpreted with caution and in conjunction with clinical and epidemiological data.

1. Specimen collection for diagnosis

The type and timing of specimen collection are important for the diagnosis of mumps virus infection. Depending on the clinical presentation and the stage of infection, different specimens may be required for optimal detection of the virus or its antibodies.

If it has been more than 3 days since symptom onset, a serum specimen for IgM detection should also be collected, in addition to a buccal swab specimen for RT-PCR . IgM antibodies are usually present within 5 days of symptom onset and may persist for up to 60 days . A serum specimen should be collected in a red-top tube or serum separator tube and allowed to clot at room temperature. The serum should then be separated by centrifugation and transferred to a sterile tube. The serum specimen should be refrigerated until shipment .

If the patient has orchitis/oophoritis, mastitis, pancreatitis, hearing loss, meningitis, or encephalitis, a buccal swab specimen for RT-PCR and a serum specimen for IgM detection should be collected, regardless of days since symptom onset . These complications may occur later in the course of infection or without parotitis, and may require additional testing to confirm mumps etiology.

Other specimens that may be useful for mumps diagnosis include urine, cerebrospinal fluid (CSF), and tissue biopsy. Urine specimens may contain mumps virus for up to 14 days after symptom onset and can be collected in sterile containers . CSF specimens may be positive for mumps virus by RT-PCR in patients with meningitis or encephalitis and can be collected by lumbar puncture . Tissue biopsy specimens may show histopathological evidence of mumps infection in affected organs and can be collected by surgical procedures .

All specimens should be labeled with the patient’s name, date of birth, specimen type, date of collection, and a unique identification number. Specimens should be accompanied by a completed CDC Specimen Submission Form (50.34) or an equivalent form from the state or local health department. Specimens should be shipped on cold packs or dry ice to the designated laboratory as soon as possible. Please contact your state or local health department to determine where to submit specimens and how to ship them .

Virus isolation is the process of growing and detecting mumps virus in cell cultures or embryonated eggs. Virus isolation can provide direct evidence of mumps infection and can be used for typing and characterization of virus strains. However, virus isolation is labor-intensive, time-consuming, and requires specialized facilities and expertise. Therefore, it is not widely used for routine diagnosis of mumps.

Cell culture

Cell culture is the most common method for virus isolation. Mumps virus can infect various types of cells derived from monkey kidney, human embryonic kidney, or human lung tissues. The preferred cell lines are Vero (African green monkey kidney), LLC-MK2 (rhesus monkey kidney), or HEp-2 (human laryngeal carcinoma).

The clinical specimens for virus isolation are usually saliva, urine, or cerebrospinal fluid (CSF). Saliva samples should be collected within the first 4 to 5 days of symptoms onset, urine samples within 2 weeks, and CSF samples within 8 to 9 days. The specimens should be inoculated shortly after collection because mumps virus is thermolabile and may lose infectivity during transport or storage.

The inoculated cell cultures are incubated at 35°C to 37°C and observed daily for cytopathic effects (CPE). Mumps virus typically causes syncytia (giant multinucleated cells) formation in cell cultures. However, not all primary mumps virus isolates show CPE, so hemadsorption techniques should be applied to detect the presence of viral hemagglutinin on the cell surface.

The identification of mumps virus in cell cultures can be confirmed by immunofluorescence assay (IFA) using mumps-specific antiserum. IFA can also provide rapid diagnosis by detecting mumps virus antigens as early as 2 to 3 days after inoculation in shell vials. Alternatively, reverse transcription polymerase chain reaction (RT-PCR) can be used to detect mumps virus genome sequences in cell cultures.

Embryonated eggs

Embryonated eggs are another method for virus isolation, especially for influenza and mumps viruses. The advantage of embryonated eggs is that they provide a large amount of virus yield and a low level of contamination by other microorganisms.

The clinical specimens for virus isolation in embryonated eggs are usually saliva or throat swabs. The specimens should be inoculated into 9- to 11-day-old embryonated chicken eggs through different routes depending on the target tissue.

The most common routes of inoculation are:

• Allantoic cavity: The allantoic cavity is the largest cavity in the egg and contains the allantoic fluid. It is mainly used for isolation of influenza viruses that grow well in this site. Mumps virus can also be inoculated into the allantoic cavity, but the growth rate is lower than in other sites.
• Amniotic cavity: The amniotic cavity is the space between the amnion and the embryo. It contains the amniotic fluid that surrounds and protects the embryo. Inoculation into the amniotic cavity is mainly done for primary isolation of influenza virus and mumps virus. Growth and replication of virus in egg embryo can be detected by hemagglutination assay.
• Yolk sac: The yolk sac is a membranous sac attached to the embryo that contains the yolk. It is also a simple method for growth and multiplication of virus. Mostly mammalian viruses are isolated using this method.

The identification of mumps virus in embryonated eggs can be confirmed by IFA or RT-PCR as described above.

Nucleic acid detection methods are based on the amplification and identification of the viral RNA using reverse transcription polymerase chain reaction (RT-PCR) or other techniques. These methods are very sensitive and specific for mumps virus and can detect the virus in various clinical samples, such as saliva, urine, cerebrospinal fluid (CSF), blood, and tissue specimens. Nucleic acid detection methods can also be used to genotype the virus and determine its molecular epidemiology.

The RT-PCR method involves extracting the viral RNA from the sample, reverse transcribing it into complementary DNA (cDNA), amplifying the cDNA using specific primers, and detecting the amplified product by gel electrophoresis, hybridization probes, or real-time fluorescence. The primers can target different regions of the viral genome, such as the nucleoprotein (NP), fusion (F), small hydrophobic (SH), or hemagglutinin-neuraminidase (HN) genes. The RT-PCR method can be performed in a single-step or a nested format, depending on the sensitivity and specificity required.

Other nucleic acid detection methods include loop-mediated isothermal amplification (LAMP), transcription-mediated amplification (TMA), nucleic acid sequence-based amplification (NASBA), and rolling circle amplification (RCA). These methods do not require thermal cycling and can be performed at a constant temperature. They also use different enzymes and mechanisms to amplify and detect the viral RNA. Some of these methods can be combined with lateral flow devices or microfluidic chips for rapid and portable diagnosis.

Nucleic acid detection methods have several advantages over virus isolation and serology for mumps diagnosis. They can provide results within hours or even minutes, whereas virus isolation can take several days. They can also detect the virus in samples that have low viral load or are negative by virus isolation. Moreover, they can differentiate between vaccine strains and wild-type strains of mumps virus, which is important for surveillance and outbreak investigation.

However, nucleic acid detection methods also have some limitations and challenges. They require specialized equipment and trained personnel, which may not be available in resource-limited settings. They are also prone to false-positive results due to contamination or cross-reaction with other viruses. Therefore, they should be performed in a quality-controlled laboratory with appropriate biosafety measures. Furthermore, they may not be able to detect novel or divergent strains of mumps virus that have mutations in the target regions. Therefore, they should be updated regularly with new primers and probes based on the circulating strains.

Nucleic acid detection methods are valuable tools for mumps diagnosis and epidemiology. They can provide rapid, accurate, and reliable results that can inform clinical management and public health interventions. However, they should be used in conjunction with other methods, such as virus isolation and serology, to confirm the diagnosis and monitor the immune status of the patients.

Serology tests are used to detect antibodies against mumps virus in the blood serum of patients. These tests can provide evidence of past or recent infection, as well as immunity status. Serology tests are usually performed using enzyme-linked immunosorbent assay (ELISA) or hemagglutination inhibition (HI) test.

ELISA is a common and sensitive method that can measure the amount of mumps-specific IgM or IgG antibodies in the serum. IgM antibodies are produced early in the infection and indicate acute or recent infection. IgG antibodies are produced later and indicate past infection or immunity. ELISA can also differentiate between antibodies induced by natural infection and those induced by vaccination.

HI test is a simple and specific method that can detect the presence of neutralizing antibodies against the hemagglutinin-neuraminidase (HN) protein of mumps virus. HI test can also measure the level of antibody titer, which reflects the degree of immunity. HI test can be used to confirm the results of ELISA or to monitor the immune response after vaccination.

Serology tests require paired sera samples from the patient: one taken during the acute phase of illness and another taken 2-4 weeks later. A fourfold or greater rise in antibody titer between the two samples indicates a recent mumps infection. A single serum sample can also be used to diagnose mumps infection if it shows a high level of IgM antibodies or a low level of IgG antibodies.

Serology tests have some limitations in diagnosing mumps infection. For example, some patients may have low or undetectable levels of IgM antibodies due to immunosuppression, delayed antibody response, or previous exposure to mumps virus. Some patients may have high levels of IgG antibodies due to cross-reactivity with other paramyxoviruses, such as measles or parainfluenza virus. Some patients may have false-positive results due to nonspecific binding of antibodies or antigens in the test system.

Therefore, serology tests should be interpreted with caution and in conjunction with clinical and epidemiological data. Serology tests should also be complemented by other laboratory methods, such as virus isolation or nucleic acid detection, for confirmation of mumps infection.

There is no specific antiviral therapy for mumps virus infection . Most people recover within 3 to 10 days. Treatment is mainly supportive and aims to relieve symptoms and prevent complications . Some of the steps that can be taken to aid recovery and lessen symptoms include:

• Rest. Getting plenty of bed rest can help the body fight off the infection .
• Fluids. Drinking enough fluids can prevent dehydration and soothe a sore throat .
• Pain relievers. Over-the-counter painkillers such as ibuprofen or acetaminophen can reduce fever, headache, and muscle aches . Aspirin should not be given to children under 16 years of age.
• Cold or warm compresses. Applying a cold or warm cloth to the swollen salivary glands can help reduce inflammation and pain .
• Soft foods. Eating soft foods that do not require much chewing can help avoid irritation of the salivary glands .
• Avoid sour foods and drinks. Sour foods and drinks such as citrus fruits, juices, and carbonated beverages can stimulate saliva production and worsen the pain of parotitis .

In addition to these measures, people with mumps should also:

• Isolate themselves. Mumps is highly contagious and can spread through respiratory droplets or direct contact with saliva or mucus of an infected person. People with mumps should stay away from school, work, or public places until at least 5 days after the onset of symptoms . They should also avoid sharing utensils, cups, or other items that may come in contact with their saliva or mucus.
• Inform their contacts. People who have been in close contact with someone who has mumps should be notified and advised to watch for symptoms of mumps or consult their health care provider if they are unsure about their vaccination status or immunity .
• Seek medical attention if complications arise. Mumps can sometimes cause serious complications such as meningitis, orchitis, oophoritis, pancreatitis, deafness, or miscarriage. If any signs of these complications occur, such as severe headache, stiff neck, abdominal pain, testicular swelling, pelvic pain, hearing loss, or vaginal bleeding, medical attention should be sought immediately .

The best way to prevent mumps is by getting vaccinated with the measles-mumps-rubella (MMR) vaccine, which provides protection against mumps as well as measles and rubella . The MMR vaccine is usually given in two doses: the first dose at 12 to 15 months of age and the second dose at 4 to 6 years of age. However, some people may need a booster dose if they are at high risk of exposure to mumps, such as during an outbreak or when traveling to areas where mumps is common . The MMR vaccine is safe and effective, but it may not work for everyone. Some people may still get mumps even if they are fully vaccinated, especially if they have a weakened immune system or are exposed to a large amount of virus . Therefore, it is important to practice good hygiene and avoid contact with people who have mumps even if vaccinated.

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