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Kaye SB, Lloyd M, Williams H, Yuen C, Scott, JA, O'Donnell N, Batterbury M, Hiscott P, and Hart CA. "Evidence for persistence of adenovirus in the tear film a decade following conjunctivitis." Journal of Medical Virology. 2005 Oct;77(2):227-31. This study investigated the prevalence of adenovirus infection 10 years after the primary infection had occurred. 304 patients with a history of adenovirus conjunctivitis 10 years earlier answered questionnaires about recurrent symptoms they had had. 20 of these patients were tested for current adenovirus infection. Samples of tears and conjunctival cells were amplified using adenovirus hexon genes and thymidine kinase primer for herpes simplex virus. The virus was sequenced and compared to the original infecting strain. Of the patients, 17/30 tested positive for adenovirus DNA (15 of whom also experienced chronic papillary conjunctivitis), 4 of which had the same serotype as they had had 10 years earlier and 2 of which had a different serotype than that of their original infection. The results of this study lend further evidence that adenoviruses can cause persistent infections, especially when the virus occurs in the ocular surfaces. Thus it is highly likely that infected individuals are vulnerable to recurrent episodes and that they may be able to transmit the virus long after original symptoms have disappeared.
Monroe, Don. "Improving Adenovirus Vaccines." The Scientist. April 4, 2005. (http://www.the-sceintist.com/news/20050404/02).
This study explored the possibility of using adenovirus as a vector to provide immunity against other pathogens. To do this, immunogenic polypeptides are added to the capsid of an adenovirus incapable of replicating and desired DNA is inserted inside the capsid. In this particular study, 720 copies of various peptides from the bacteria Pseudomonas aerunginosa were added to the capsid of the adenoviral vector (many different bacteria peptides were studied, but the strongest immune response was provided by Epi8, a 14 amino acid segment that is highly evolutionarily conserved.) Most of the mice treated with this vaccine survived after pulmonary infection with the P. aeruginosa bacteria while all of the untreated mice died within a few days. A second "booster" dose of the vaccine provided even greater immunity. Although adenoviruses have long been studied as potential vectors for gene therapy or vaccination, this study demonstrated a more efficient and specific immune response against the pathogen than previous vaccines.
Benefits of this vaccine include the low dosage necessary to provide immunity, ease of delivery, safety of vaccine, and low cost of production. Vaccines using adenoviral vectors hold much promise in general, but efficient vaccines targeted for the respiratory tract hold special promise for CF patients, or other suffering from acute respiratory disease.
L. Lenaerts, E. Verbeken, E. De Clercq, and L Nasens. "Mouse Adenovirus Type 1 Infection in SCID Mice: an Experimental Model for Antiviral Therapy of Systemic Adenovirus Infections." Antimicrobial Agents and Chemotherapy. Nov 2005, p. 4689-4699, Vol 49, No 11. The goal of this study was to develop better treatments for systemic adenoviral infections in immunocompromised hosts. To do this, SCID mice were infected with MAV-1 (mouse adenovirus type 1), which caused a fatal disseminated infection which led to hemorrhagic enteritis and death within 19 days. Analysis of the mice showed that the virus had spread throughout the lungs, brain, liver, spleen, intestine, heart, and kidney. A subset of infected mice was treated with the antiviral drug, cidofovir (100 mg/kg body weight). This treatment delayed death, but could not prevent it. The results of this study indicate that antiviral drugs can aid in the treatment of adenoviral infections, but these treatments need to be modified to elicit a more efficient adaptive immune response if they are to provide lasting benefits.
Gray CG, Setterquist SF, Jirsa SJ, DesJardin LE, Erdman DD: Emergent strain of human adenovirus endemic in Iowa. Emerg Infect Dis. 2005 Jan. http://www.cdc.gov/ncidod/EID/vol11no01/04-0490.htm. This study evaluated 76 adenovirus serotype 7 samples collected from Iowa from 1992 to 2002. Beginning in 1992 adenovirus serotype Ad7d2 became increasingly more prevalent across Iowa and began replacing Ad7b, the predominant adenovirus serotype that had been circulating in the U.S. since the early 1970s. And by 2002, Ad7d2 replaced all other Ad7 serotypes in Iowa. This finding is quite significant because Ad7d2 seems to be more virulent than other Ad7 serotypes. Ad7d2 has been associated with epidemics of unusually severe respiratory disease with high fevers among children. Thus, there is a danger of Ad7d2 migrating to new areas and causing severe epidemics in unprotected populations.
Choi EH, Kim HS, Eun BW, Kim BI, Choi JY, Lee HJ, et al.: Adenovirus type 7 peptide diversity during outbreak, Korea, 1995–2000. Emerg Infect Dis. 2005 May. http://www.cdc.gov/ncidod/EID/vol11no05/04-1211.htm. This study analyzed the genome characteristics of adenovirus serotype 7, which was isolated in outbreaks in Korea from 1995 to 2000. Phylogenic trees based on hexon, fiber, and gene E4 suggests that the Ad7 epidemic in Korea was caused by introduction of Japanese Ad7d strains.