The keys to this question are the terms "universally useful" and "infective." Some of the described methods lead to the counting of both viable and nonviable particles, as described below.

Electron microscopy is useful for enumerating purified virus particles present at high density. The addition of a known number of latex particles to the suspension, followed by the calculation of the ratio of those particles to viral particles, provides an accurate count. Of course, this technique has the disadvantage that viable and nonviable particles cannot be differentiated. Equally important, very few diagnostic laboratories, and indeed not all research laboratories, have ready access to an electron microscope.

The plaque assay is the most precise measure of infectivity. The basis of this technique is the formation of clear zones, plaques or foci, in a monolayer of host cells. Serial dilutions of the virus are added to a monolayer of cells known to be infected by the cells (for example, MDCK cells are used for influenza). Most commonly after the virus has been allowed to adsorb onto the cells, an agar overlay is added to prevent dispersion of the virus. This ensures that each plaque represents only a single initial virus particle. For viruses which only infect contiguous cells without releasing virions into the surrounding medium, the agar may be replaced by a liquid.

Certainly not applicable for all viruses, the pock assay involves the counting of localized lesions (pocks) that form on the chorioallantoic membrane (CAM) of the embryonated egg upon addition of known dilutions of the virus. As in the plaque assay, each lesion represents a single original virus particle.

Instead of providing a quantitative measure of viral infectivity, quantal assays provide only a "yes or no" result. In quantal assays, each viral replication cycle results in an amplification of the effects of each individual virus particle. The virus is serially diluted, and appropriate cells are incubated with a known volume of each dilution. The endpoint for these assays may be negative effects, including morbidity in animals and development of lesions on either the chorioallantoic membrane or on the embryo of eggs. Following the incubation period, each target animal, or sample, is examined for a +/- response.

Epstein-Barr virus and cytomegalovirus elicit a large T-cell response, resulting in a mononucleosis-like syndrome. EBV infection is subclinical and milder in children than adolescents or adults. EBV initiates infection in the epithelial cells of the oropharynx and then spreads to the B lymphocytes in lymphatic tissue and blood. Classical lymphocytosis is associated with the activation and proliferation of suppressor T cells, and it leads to infectious mononucleosis. The atypical lymphocyte, also known as "Downey cells", increases in peripheral blood during the second week of infection. Major T-cell response causes swollen lymph glands, spleen, and liver. Fever, malaise, fatigue, pharyngitis, lymphadenopathy, and hepatosplenomegaly are the classical symptoms associated with infectious mononucleosis.

Cytomegalovirus is associated with heterophile-negative mononucleosis. Polyclonal B cell activation by EBV leads to production of heterophile antibodies, which can be detected by the end of first week of infection and last for several months.

Respiratory syncytial virus, varicella zoster virus, and influenza virus are not associated with infectious mononucleosis.

Except for the Reoviridae, which contains the orbiviruses, rotaviruses, and reoviruses, all of the families mentioned are DNA viruses. The Parvoviridae and Adenoviridae families contain the Parvovirus and Adenovirus, respectively. The viruses in both of these families have a naked virion (i.e., without an envelope), but viruses in the former family have a complex nucleocapsid structure, while those in the latter family have an icosahedral nucleocapsid symmetry. The herpes simplex virus, cytomegalovirus, Varicella -Zoster virus, and the Epstein-Barr virus all belong to the Herpesviridae family. The family of Poxviridae contains complex viruses with a naked virion, such as the vaccinia, smallpox, and variola viruses.

Rickettsia, chlamydia, prions, and viroids can be distinguished from viruses, but not by just one of the mentioned criteria. While all of these groups are obligate intracellular organisms, only the viruses are parasites with an absolute intracellular requirement, which also depend on the machinery of the host cell for replication. Prions are small infectious protein particles. Viroids are subviral infectious nucleic acids, which lack even the protein capsid found in viruses. Viruses may contain a genome of DNA or RNA, so the presence of an RNA genome is indicative of a virus, but the presence of a DNA genome is not.

Hepatitis C is an enveloped icosahedral RNA virus with gene order characteristic of the family Flaviviridae. The genome of Hepatitis C is infectious and consists of a linear single stranded 9.5 kb molecule of RNA. The virus replicates in the cytoplasm. Hepatitis C is transmitted by paranteral and sexual routes. It is the most common cause of post-transfusion hepatitis. Hepatitis C is associated with acute infection, chronic liver disease, and cirrhosis. Hepatitis C viral infection may serve as a predisposing factor in primary hepatocellular carcinoma.

Hepatitis B virus is an enveloped DNA virus that is part of the Hepadnaviridae family. The genome of Hepadnaviridae family is characterized by the presence of a circular, partially double stranded DNA molecule. Hepatitis B virus consists of a icosahedral core within a closely adherent capsid that contains cellular lipid, glycoproteins, and a virus-specific surface antigen called Hepatitis B surface antigen (HBsAg). The virus encodes a reverse transcriptase and replicates through an RNA intermediate. Hepatitis B virus shows tropism to the liver and replicates in hepatocytes. Hepatitis B is also called serum hepatitis and is caused by a DNA virus known as hepatitis B virus. It is transmitted by parenteral or sexual routes. Hepatitis B has a longer incubation period, which is approximately 50-160 days. Onset of the disease is gradual and the infection can be acute or self-limiting or can lead to persistent viremia and chronic liver disease with immunologic complications.

The Hepatitis A virus is a naked icosahedron that is member of the Picornaviridae family. The genome of this virus is infectious and contains a single linear molecule of single stranded RNA. Hepatitis A is transmitted by feco-oral routes and was known as infectious hepatitis. The virus enters the body by ingestion and multiplies in intestinal epithelial cells. The virus then enters the circulation and invades parenchymal cells in the liver. Incubation period for Hepatitis A is 15-40 days.

Hepatitis D virus is a very small virus with tiny genome and is classified under genus Deltavirus. It is defective satellite virus and needs Hepatitis B virus as helper, i.e., it is infective only in the presence of Hepatitis B virus. The outer capsid of the virion contains Hepatitis B surface antigen, which is encoded by HBV co-infecting the same cell.

Hepatitis E virus is a naked virus, which has icosahedral capsid with surface depression. Hepatitis E virus is from the family Calciviridae and contains a single molecule of a single stranded RNA. Hepatitis A is transmitted by feco-oral routes and by contaminated food and water. Hepatitis E is associated with cholestasis and has a higher fatality rate in pregnant women.

Hepatitis A virus and Hepatitis E virus are not associated with the following:

• Parenteral transmission
• Chronic carrier state
• Chronic hepatitis
• Cirrhosis
• Hepatocellular carcinoma

Hepatitis B virus, Hepatitis C virus, and Hepatitis D virus are associated with the following:

• Parenteral transmission
• Chronic carrier state
• Chronic hepatitis
• Cirrhosis
• Hepatocellular carcinoma

Coxsackievirus type A and coxsackievirus type B are members of the Picornaviridae family. Coxsackievirus type A is associated with herpangina,which is commonly seen in children. Herpangina is a severe febrile pharyngitis characterized by vesicles or nodules primarily on the soft palate. The majority of cervical cancers (approximately 90%) contain human papilloma virus DNA, usually of type 16 or 18.

Hepatitis B virus (HBV) is a human carcinogen associated with hepatocellular carcinoma. The incidence of hepatocellular carcinoma is higher in a person who becomes infected with HBV earlier in life. Herpes simplex virus type 1 (HSV-1) is a member of the Herpes viridae family and consists of a double stranded DNA genome. Primary infection with HSV-1 mostly involves the mouth and/or throat. Gingivostomatitis is a classic clinical presentation of HSV-1 infection. Variola virus is a brick-shaped virus with a single linear molecule of double stranded DNA and is a member of the Poxviridae family. Variola virus was the causative agent of smallpox that multiplied in the lymph nodes.

All of the families mentioned are RNA viruses. The Picornaviridae family contains viruses that lack an envelope and are icosahedral (rather than helical) in morphology. The Picornaviridae family contains enterovirus, cardiovirus, and rhinovirus. The Orthomyxoviridae family contains the influenza virus, while the Paramyxoviridae family contains the parainfluenza virus. The Rhabdoviridae and Coronaviridae families contain the rabies virus and Coronaviruses, respectively.

The child has the characteristic symptoms of laryngotracheobronchitis, commonly known as croup.

All of the listed viruses can cause respiratory tract infections in infants and young children, each producing different clinical manifestations. Parainfluenzavirus is the most common agent of croup. Types 1 and 2 are particularly associated with this disease. Croup is characterized by respiratory obstruction due to swelling of the larynx and related structures. Infection may spread deeper to the lower trachea and bronchi, culminating in pneumonia and bronchitis. The infection is seen mostly in 6- to 18-month-old children.  

Respiratory syncytial virus is mostly associated with bronchiolitis and pneumonia. Influenza virus is also one of the agents of laryngotracheitis in infants, though not as frequently as the parainfluenza viruses. The virus can be responsible for pneumonia in infants. Adenoviruses cause common cold-like symptoms and upper respiratory tract infection. Certain serotypes, particularly types 3, 7 and 21, cause pneumonia in children. Mortality rates are higher in the very young. Rhinoviruses are agents of common cold.

Antigenic shift and antigenic drift can be found in the influenza virus.  Antigenic shift is a process by which 2 or more different types of influenza A combine to form a virus radically different from the ancestor strains. Antigenic shift occurs in 2 ways.

1. Antigenic shift can occur through genetic recombination, or reassortment, when 2 or more different influenza A viruses infect the same host cell and combine their genetic material.
2. Qn influenza A virus can jump from 1 type of organism, usually a bird, to another type of organism, such as a human, without undergoing major genetic change.

A point mutation that leads to an amino acid change and altered antigenic sites so that the virus is no longer recognized by the host immune system is called antigenic drift. Peptidoglycan and teichoic acids are components of the bacterial cell wall and prions are infectious protein particles.

Hepatitis E virus is a naked (+) strand, ssRNA virus. It has clinical and biochemical features that are very similar to Hepatitis A, except that it seems to be more severe in pregnant women. Therefore, Hepatitis E is the virus that is most likely the cause of disease in this case, if serology indicated the absence of Hepatitis A.

The other choices are incorrect. Hepatitis C is enveloped and does not cause gastrointestinal symptoms. Rhinovirus causes common cold. Rotavirus does not present with jaundice as do hepatitis-causing viruses. Last, yellow fever can be associated with hepatitis, but it is a lot more severe in presentation than Hepatitis A and is transmitted by mosquitoes, not fecal-orally.