Israel Medical Association Journal

Background: The evaluation of influenza vaccine activity and potency are based on the immune response to hemagglutinin, and protection is indicated when a ≥ 1:40 titer of hemagglutination inhibition serum antibody is present. Neuraminidase, the second surface glycoprotein, may also have a role in protection, but little information on the immunologic response to this component is available.

Objectives: To determine whether any response to neuraminidase is evoked by intranasal immunization with a novel, whole, inactivated anti-influenza vaccine.

Methods: This study was part of a more comprehensive study of mucosal and serum immune response to this vaccine. Fifty-four young adults were immunized intranasally, 9 intramuscularly and 18 received a placebo. Twenty-three elderly people were immunized intramuscularly, and 21 elderly and 17 children were immunized intranasally. Serum and nasal antibodies to antigens N1 and N2 were determined by the lectin neuraminidase test.

Results: Serum response following intranasal vaccination was lower than after intramuscular vaccination, and ranged from 21.4 to 35.3% and 33.3 to 64.7% following intranasal vaccination and 52.2 to 77.8% and 47.8 to 88.9% after intramuscular vaccination, to N1 and N2 respectively. Nasal antibody response was low and was found only after intranasal vaccination, and response to N2 was better than to the N1 antigen.

Conclusions: It may be beneficial if future vaccines would include competent hemagglutinin and neuraminidase, which would afford a higher level of protection.
 

Background: While most allelic pairs of DNA replicate synchronously during the S phase of the cell cycle, some genes normally replicate asynchronously, i.e., genes on the X chromosome and imprinted genes. The replication control mechanism is unknown but was shown to be impaired in malignancies and chromosomal trisomies where replication pattern becomes asynchronous.

Objectives: To determine the level of asynchronization in replication timing of cells from patients with microdeleted genomes.

Methods: We applied monocolor fluorescent in situ hybridization with different probes on leukocytes from microdeleted genomes.

Results: All samples derived from the microdeleted genomes showed significantly higher levels of an asynchronized pattern compared to normal individuals.

Conclusions: Even a “small” genetic imbalance (microdeletion) can interfere with gene replication and cell cycle progression, as previously shown in full trisomies.