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Retrograde and anterograde spread of virus in nerves. (A) Anterograde spread of infection. The virus invades at dendrites or cell bodies and reproduces. Virus particles then spread to axon terminals, where they cross synaptic contacts to invade dendrites or cell bodies of the second neuron. (B) Retrograde spread of infection. The virus invades at axon terminals and spreads to the cell body, where reproduction occurs. Progeny virus particles spread to a neuron at sites of synaptic contact. Particles enter the axon terminal of the second neuron to initiate a second cycle of replication and spread. (C) Identification of a possible micro circuit in the rodent visual cortex (V2) after injection of a green fluorescent protein-expressing strain of pseudorabies virus into the synaptically connected, but distant, V1 region. Infection spread via V1 axons (V1 cell bodies are located far out of the field of view) in a retrograde manner to a subset of V2 cell bodies is seen here. Confocal microscopy and image reconstruction by Botond Roska, Friedrich Miescher Institute, Basel, Switzerland.

Those who study virus spread in the nervous system often use the words retrograde and anterograde to describe direction. Confusion can arise because the terms can be used to describe directional movement of virus particles inside a cell, as well as spread between synaptically connected neurons. Spread from the primary neuron to a second-order neuron in the direction of the nerve impulse is called anterograde spread (see figure). Spread in the opposite direction is termed retrograde. Spread inside a neuron is defined by microtubule polarity. Anterograde transport occurs on micro tubules from the cell body toward the axon terminus; retrograde spread occurs from the axon terminus toward the cell body.

 Ekstrand MI, Enquist LW, Pomeranz LE. 2008. The alpha-herpesviruses: molecular pathfinders in nervous system circuits. Trends Mol Med 14:134–140.

Figure 2.17 Outline of the spread of alphaherpesviruses and relationship to disease. Although herpes simplex virus can infect many cell types, in most infected individuals, it remains restricted to the local site of infection and establishes latency in the ganglia that innervate that site. Under conditions when the host has a weakened immune system, viremia can result in which distal organs become infected and/or the virus may transition from the peripheral nervous system (PNS) to the central nervous system (CNS); again, this is a rare event.

Figure 2.18 Blood-tissue junction in a capillary, venule, and sinusoid. (Left) Sinusoids, lined with macrophages of the reticuloendothelial system, as found in the adrenal glands, liver, spleen, and bone marrow. (Center) Fenestrated endothelium found in the choroid plexus, villi of the intestine, renal glomerulus, pancreas, and endocrine glands. (Right) Continuous endothelium and basement membrane found in the central nervous system, connective tissue, skeletal and cardiac muscle, skin, and lungs. Adapted from Mims CA et al. 1995. Mims’ Pathogenesis of Infectious Disease (Academic Press, Orlando, FL).

Figure 2.19 How viruses gain access to the liver. Two layers of hepatocytes are shown, with the sinusoid at the center, lined with kupffer cells. On the left, transcytosis through the kupffer cells is shown; on the right, direct kupffer cell infection is illustrated, followed by infection of underlying hepatocytes. Viruses not taken up by either route will flow through. Adapted from Mims CA et al. 1995. Mims’ Pathogenesis of Infectious Disease (Academic Press, Orlando, FL).