Indications, usage, and dosage of the transfer factor.

The transfer factor (TF) was described in 1955 by S. Lawrence. In 1992 Kirkpatrick characterized the specific TF at molecular level. The TF is constituted by a group of numerous molecules, of low molecular weight, from 1.0 to 6.0 kDa. The 5 kDa fraction corresponds to the TF specific to antigens. There are a number of publications about the clinical indications of the TF for diverse diseases, in particular those where the cellular immune response is compromised or in those where there is a deficient regulation of the immune response. In this article we present our clinical and basic experiences, especially regarding the indications, usage and dosage of the TF. Our group demonstrated that the TF increases the expression of IFN-gamma and RANTES, while decreases the expression of osteopontine. Using animal models we have worked with M. tuberculosis, and with a model of glioma with good therapeutic results. In the clinical setting we have worked with herpes zoster, herpes simplex type I, herpetic keratitis, atopic dermatitis, osteosarcoma, tuberculosis, asthma, post-herpetic neuritis, anergic coccidioidomycosis, leishmaniasis, toxoplasmosis, mucocutaneous candidiasis, pediatric infections produced by diverse pathogen germs, sinusitis, pharyngitis, and otits media. All of these diseases were studied through protocols which main goals were to study the therapeutic effects of the TF, and to establish in a systematic way diverse dosage schema and time for treatment to guide the prescription of the TF.

Comparison of two methods of PCR followed by enzymatic restriction digestion for detection and typing of herpes simplex viruses isolated from patients with mucocutaneous or cutaneous lesions.

A multitude of different polymerase chain reactions (PCRs) have been described for detection and typing of Herpes simplex virus (HSV). This paper compares two PCRs coupled to enzymatic restriction (PCR/RFLP) to detect and type HSV. A primers set was designed to amplify a HSV DNA fragment from UL30 and UL 15 genes. Typing was done by restriction of the UL30 and UL15 amplicons with Ava II and Hpa II enzymes, respectively. This strategy was tested with two reference strains (HSV-1 McIntyre, and HSV-2 G), and 47 clinical HSV isolates. Both PCRs produced the expected amplicons (a 492 bp UL30, and 305 bp UL15). The restriction of both amplicons clearly differentiated HSV- from HSV-2, and produced equal results. Thirty one (66%) of the isolates were identified as HSV-1, and the other 16 (34%), as HSV-2. Most of the HSV-1 isolates (27/31) were from orofacial and thoracic lesions; and also, one half of the HSV-2 isolates (8/16) were from the same anatomical regions. Our results showed that either of the two PCR/RFLP could be used to detect and type HSV. Furthermore, our results of the anatomical site of HSV-1 and HSV-2 infections are consistent with previous reports which have shown changes in the classical anatomical localization of herpesvirus infections.